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Year 3 - Reproduction > Complications of pregnancy, labour and twins > Flashcards

Complications of pregnancy, labour and twins Flashcards

1
Q

How can you clinically assess fatal growth?

A

Symphysiofundal height (in cms) - Measuring from symphysis pubis to the top of the fundus of the uterus – may not be central

note - turn the measuring tape upside down to reduce bias

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2
Q

How can you interpret symphysiofundal height?

A

Should be usually + or - 3cms of gestational age in weeks

e.g. At 32 weeks, a normal measurement would be 29 to 35 cms

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3
Q

What investigation would you do if you suspect the baby is large or small for dates?

A

Ultrasound scan

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4
Q

What measurements would you do on an ultrasound scan?

A

> Abdominal circumference
Femur length
Head circumference

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5
Q

What can cause a foetus to be small for date?

A 
> Low BMI, maternal build
> Age
> Ethnicity, familial/ genetic
> Social class
> Smoking
> Substance misuse       
> Alcohol use – fetal alcohol syndrome

> Maternal disease:

  • Preeclampsia
  • Chronic hypertension
  • Severe asthma
  • Autoimmune disorders eg SLE, antiphospholid syndrome
    - Repeated antepartum haemorrhages

> Infections – Toxoplasma, CMV etc

> Fetal abnormality (eg gastroschisis), chromosomal abnormality like triploidy, Turners XO

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6
Q

What can cause a foetus to be large for date?

A

> Parity (multiparity)

> Ethinicity / familial / Genetic / social class

> Maternal diabetes

> Polyhydramnios:

  • Maternal diabetes
  • Fetal abnormality eg duodenal atresia, tracheo esophageal fistula
  • Unexplained

> Multiple pregnancy

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7
Q

What tests would do to confirm fetal well being?

A

> Confirm good fetal movement

> Fetal Cardiotocograph (CTG)

> Good Doppler blood flow in umbilical artery on scan

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8
Q

What happens to mortality rates as there is an increase in number of babies in a multiple pregnancy e.g. twins, triplets etc?

A

Increases

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9
Q

What happens to cerebral palsy rates as there is an increase in number of babies in a multiple pregnancy e.g. twins, triplets etc?

A

Increases

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10
Q

What happens to average pregnancy length as there is an increase in number of babies in a multiple pregnancy e.g. twins, triplets etc?

A

Decreases

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11
Q

What happens to average birth weights as there is an increase in number of babies in a multiple pregnancy e.g. twins, triplets etc?

A

Decreases

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12
Q

What is chorionicity?

A

In a twin or multifetal pregnancy, the number of chorions in the placenta that supply blood and nourishment to the developing fetuses.

Twins sharing a common placenta may experience twin-twin transfusion syndrome; those with separate blood supplies have, on average, fewer perinatal health problems.

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13
Q

What is zygosity?

A

In the case of twins, whether developing from one zygote (monozygotic twins) or two zygotes (dizygotic twins).

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14
Q

What can lead to Twin to Twin Transfusion syndrome?

A

When there is chorionicity

Twins sharing a common placenta may experience twin-twin transfusion syndrome. There is an arteriovenous shunt in place.

Those with separate blood supplies have, on average, fewer perinatal health problems.

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15
Q

What is Dichorionic Diamniotic twins?

A

Two separate placenta and two sacs

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16
Q

What is Monochorionic Monoamniotic twins?

A

One sac and one placenta

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17
Q

Two sacs with one fused looking placenta - what is this called?

A

Either:

  • Dichorionic diamniotic
  • Monochorionic diamniotic
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18
Q

On an ultrasound what does a T sign indicate?

A

Monochorionic

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19
Q

On an ultrasound what does a Lamda sign indicate?

A

Dichorionic

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20
Q

What is the natural rate of twinning?

A

1:90

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21
Q

What is the incidence of monozygotic twins?

A

4:1000 pregnancies

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22
Q

What can cause an increase in the incidence of dizygotic twins?

A 
> Increase of age
> Parity 
> Weight 
> Height 
> Familial
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23
Q

What can cause an increase in the incidence of monozygotic twins?

A

There is a constant rate of 4:1000 pregnancies

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24
Q

When is multiple pregnancy suspected?

A
  • Large for date uterine size
  • Multiple fetal heart rates are detected
  • Multiple fetal parts are felt
  • HCG & maternal serum alpha-fetoprotein is elevated for gestational age
  • Pregnancy with ART (Assisted reproduction technique)
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25
Q

How is multiple pregnancy confirmed?

A

Ultrasound

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26
Q

Monozygotic versus Dizygotic?

A

Monozygotic = One egg leads to twins (identical)

Dizygotic = Two eggs (ova) lead to twins (Non-identical)

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27
Q

Which type of twins are more common?

A

Dizygotic = 70-80% of all twins

Two eggs (ova) lead to twins (Non-identical)

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28
Q

What is the rate of monozygotic twins in all twins?

A

20-30% of all twins

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29
Q

What is the rate of monozygotic twins in all twins?

A

70-80% of all twins

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30
Q

How does monozygotic twins occur?

A

The cleavage of a single fertilised ova

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31
Q

What determines placentation of monozygotic twins?

A

The timing of the cleavage of the single fertilised ova determines plancentation

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32
Q

Which type of monozygotic twins has the lowest mortality rate?

A

Dichorionic/diamniotic monozygotic twins <10% mortality rate

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33
Q

When does cleavage occur to allow production of Dichorionic/diamniotic monozygotic twins?

A

Cleavage of the fertilised ova must occur within the first 3 days after fertilisation

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34
Q

What does it mean for monozygotic twins to be Dichorionic/diamniotic?

A

Each fetus will be surrounded by amnion & chorion (each fetus has its own placenta), much like dizygotic twins

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35
Q

What does it mean for monozygotic twins to be monochorionic/diamniotic?

A

Share single placenta but separate amniotic sac

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36
Q

What does it mean for monozygotic twins to be monochorionic/monoamniotic?

A

Share single placenta & single sac

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37
Q

Which type of monozygotic twins has the highest rate of mortality?

A

Monochorionic/monoamniotic
= Share single placenta & single sac

A mortality of 50-60%

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38
Q

What is the rate of Monochorionic/monoamniotic monozygotic twins?

A

<1%

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39
Q

When does cleavage occur to allow production of monochorionic/diamniotic monozygotic twins?

A

Cleavage occurs between days 4 and 8 after fertilisation

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40
Q

When does cleavage occur to allow production of monochorionic/monoamniotic monozygotic twins?

A

Cleavage occurs after the 8th day, usually between days 9-12

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41
Q

What is the mortality rate of monochorionic/diamniotic monozygotic twins?

A

Mortality of 25% in monochorionic/diamniotic monozygotic twins

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42
Q

If cleavage of monozygotic twins does not occur until after 12 days what is likely to occur?

A

Cleavage after 12 days

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43
Q

What is the incidence of conjoined twins?

A

1:70,000 deliveries

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44
Q

What is the most common types of fusion in conjoined twins?

A

Chest and/or abdomen

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45
Q

Which type of monozygotic twins can lead to twin-twin transfusion?

A

They need to be monochorionic so therefore:
1) Monochorionic / diamoniotic

2) Monochorionic / monoamniotic

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46
Q

Complications of multiple pregnancy?

A
  • High perinatal mortality & morbidity (3-4 times higher than singleton pregnancy)
  • Abortion(<50% of twins diagnosed in the first trimester result in live birth(vanishing twin))
  • Nausea & vomiting
  • Preterm labour (50%)(twins delver at 37 weeks, triples at 33 weeks, Quadruplets at 29 weeks)
  • IUGR
  • PET (3 times higher than singleton)
  • Polyhydramnios ( in 10%)
  • Congenital anomalies
  • Postpartum hemorrhage
  • Placental abruption, placenta previa
  • Discordant twin growth ( more than 20%discrepacy in fetal weights)
  • Malpresentation, cord prolapse, Operative delivery
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47
Q

Causes of perinatal mortality & morbidity?

A
  • Prematurity (Respiratory distress syndrome)
  • Birth trauma
  • Cerebral hemorrhage
  • Birth asphyxia
  • Congenital anomalies
  • Still birth
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48
Q

What is the rate of twin-twin transfusion syndrome in monochorionic twins?

A

20-25%

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49
Q

Within twin-twin transfusion syndrome what happens to the recipient?

A

The recipient fetus will have heart failure, polyhydramnios, and hydrops

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50
Q

Within twin-twin transfusion syndrome what happens to the donor?

A

The donor will have IUGR & oligohydramnios

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51
Q

How would you manage twin-twin transfusion syndrome?

A

Management includes:
1) Amnio-reduction of the receipient twin

2) Intra-uterine blood transfusion for the donor twin
3) Selective fetal reduction
4) Fetoscopic laser ablation of placental anastomosis

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52
Q

How should you antenatally manage a multiple pregnancy?

A

> Adequate nutrition (300 additional calories per day per fetus)

> Prevent anemia

> More frequent antenatal visits

> Ultrasound:

  • Assess chorionicity at 9-10 weeks
  • Nuchal translucency at 12-13+ weeks
  • Assessment of fetal growth & fetal wellbeing every 3-4 weeks from 23 weeks onward

> Multifetal reduction may offered for high order multiple gestation in the first trimester

> Preterm labour risk:

  • Serial cervical length assessment
  • Steroids for fetal lung maturation
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53
Q

What can be assessed in chronionicity by ultrasound in multiple pregnancy?

A 
> Multiple gestational sacs
> Conjoined twins
> 2 yolk sacs
> 2 gestational sacs
> Twin peak sign (Lambda) Dichorionic twins
> T sign monochorionic twins
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54
Q

What does twin peak sign indicate?

A

Twin peak sign = Lambda

Indicates Dichorionic twins

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55
Q

Management of labour in multiple pregnancy - lie of first foetus is cephalic?

A

Usually normal delivery

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56
Q

Management of labour in multiple pregnancy - lie of first foetus is non vertex?

A

Cesarean section

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57
Q

Management of labour in multiple pregnancy - lie of foetus locked (Breech-vertix)?

A

Cesarean section

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58
Q

What dictates the management of labour in multiple pregnancy?

A

Depends on presentation, gestational age, presence of fetal complications, experience of the obstetrician

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59
Q

What is shoulder dystocia?

A

Shoulder dystocia is when the baby’s head has been born but one of the shoulders becomes stuck behind the mother’s pubic symphysis

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60
Q

What is the dangers of shoulder dystocia?

A

> Damage to the brachial plexus

> Umbilical cord entrapment

> Severe brain damage or death due to hypoxia or acidosis if delay in delivery

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61
Q

Management of Shoulder Dystocia?

A

HELPERR:
1) H – Call for Help

2) E – Evaluate for Episiotomy
3) L – Legs (McRoberts Position)
4) P – Suprapubic Pressure
5) E – Enter Manouvers (Internal Rotation)
6) R – Remove the Posterior Arm
7) R – Roll the Patient (Onto all Fours)

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62
Q

What causes postpartum haemorrhage?

A

1) Thrombin causes
2) Tissue causes
3) Tone causes
4) Trauma causes
5) Other causes

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63
Q

What causes postpartum haemorrhage - Thrombin?

A

> Pre-eclampsia
Placental abruption
Pyrexia in labour
Bleeding disorders

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64
Q

What causes postpartum haemorrhage - Tissue?

A

> Retained placenta
Placenta accreta
Retained products of conception

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65
Q

What causes postpartum haemorrhage - Tone?

A

> Placenta praevia
Over distention of the uterus, multiple pregnancy, polyhydramnios, macrosomia
Uterine relaxants
PPH

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66
Q

What causes postpartum haemorrhage - Trauma?

A

> Caesarean section
Episiotomy
Macrosomia (>4kg baby)

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67
Q

What causes postpartum haemorrhage - Others?

A 
> Asian ethnicity 
> Anaemia
> Induction
> BMI >35
> Prolonged labour 
> Age
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68
Q

What is primary postpartum haemorrhage?

A

In the first 24 hours after delivery >500ml blood loss

  • > 500 is common 1/20
  • Severe haemorrhage, >2000ml, is rare 6/1000
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69
Q

What is secondary postpartum haemorrhage?

A

> 24 hours to up to 6 weeks post delivery (Often caused by RPOC)

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70
Q

What is more common primary or secondary postpartum haemorrhage?

A

Primary which is 99% of all PPH

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71
Q

Management of primary postpartum haemorrhage?

A 
> Call for help!
> ABCDE...
> Empty Bladder
> Rub up fundus
> Drugs
> Surgical 
> Manage on clinical signs not just EBL
> Fluid Replacement +/- Blood Products.
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72
Q

Management of primary postpartum haemorrhage - drugs?

A

1) Oxytocin 5iu slow iv injection
2) Ergometrine 0.5mg slow iv injection (not in HTN)
3) Oxytocin infusion
4) Carboprost 0.25mg im (max 8 doses
5) Misoprostol 800 micrograms

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73
Q

Management of primary postpartum haemorrhage - Surgical?

A

> Surgical:

1) Intrauterine Balloon tamponade
2) Interventional Radiology
3) B-Lynch Suture
4) Hysterectomy

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74
Q

What is cord prolapse?

A

Cord prolapse - the descent of the umbilical cord through the cervix alongside (occult) or past (overt) the presenting part in the presence of ruptured membrane.

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75
Q

What is the overall incidence of cord prolapse?

A

0.1-0.6%

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76
Q

Risk factors of cord prolapse - general?

A 
> Multiparity
> Low birthweight (<2.5 kg)
> Preterm labour <37 weeks 
> Fetal congenital anomalies
> Breech presentation
> Transverse, oblique and unstable lie 
> Second twin
> Polyhydramnios
> Unenganged presenting part 
> Low-lying placenta
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77
Q

Risk factors of cord prolapse - procedure related?

A

> Artificial rupture of membranes with high presenting part
Vaginal manipulation of the foetus with ruptured membranes
External cephalic version (during procedure)
Internal podalic version
Stabilising induction of labour
Insertion of intrauterine pressure transducer
Large balloon Cather induction of labour

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78
Q

Management of cord prolapse?

A

> Call for Help!

> Replace cord into vagina (not uterus)

> Perform digital elevation of the presenting part

> Catheterise and fill bladder to elevate presenting part.

> Encourage mother to adopt Knee-Chest or left lateral position with raised hips

> Consider tocolysis

> Arrange for a Category 1 C-Section

> Use a gloved hand in the vagina to push the foetus up and off the cord

> Knee-chest (90o angle) position uses gravity to shift the foetus out of the pelvis

> Elevate the woman hips using two pillows and Trendelenburg (head down) position

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79
Q

How often is there failure to start abut?

A

Approx 1 in 5 pregnancies

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80
Q

What is the risks of use of prostaglandin/oxytocin to induce labour?

A

Risk of uterine hyperstimulation

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81
Q

What indications are there for induction of labour?

A

1) Diabetes (usually before due date)
2) Post dates – Term + 7 days
3) Maternal health problem that necessitates planning of delivery e.g. on treatment for DVT
4) Fetal reasons e.g. growth concerns, oligohydramnios

5) You may also see IOL for :
- social
- maternal request
- pelvic pain
- “big” babies

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82
Q

What is induction of labour?

A

Induction of labour is when an attempt is made to instigate labour artificially using medications and/or devices to “ripen cervix” followed usually by artificial rupture of membranes (performing an amniotomy)

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83
Q

What is the Bishops’s score?

A

The Bishop’s score is used to clinically assess the cervix.

The higher the score, the more progressive change there is in the cervix and indicates that induction of labour is likely to be successful.

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84
Q

What does the Bishops’s score use to asses the cervix?

A

1) Dilatation (in cm)
2) Length of cervix (in cm) (Effacement)
3) Position
4) Consistency
5) Station (in cm)

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85
Q

If cervix is not dilated and effaced (Low Bishop’s score) what can be done to induce labour?

A

Vaginal prostaglandin pessaries / Cook Balloon can be used to ripen (open) the cervix

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86
Q

Once cervix has dilated and effaced what is done next to induce labour?

A

An amniotomy can be performed

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87
Q

What is amniotomy?

A

Amniotomy is the artificial rupture of the fetal membranes (“waters”) usually using a sharp device e.g. amniohook

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88
Q

Once amniotomy has been performed what is used next to allow induction of labour?

A

Once amniotomy performed, IV oxytocin can be used to achieve adequate contractions – aim for 4-5 contractions in 10 minutes

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89
Q

What are causes of inadequate progress in labour?

A 
> Cephalopelvic 
disproportion (CPD)
> Malposition
> Malpresentation
> Inadequate uterine activity
> Other reasons for obstruction (e.g. ovarian cyst or fibroid)
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90
Q

How is progress of labour evaluated?

A

Progress in labour is evaluated by a combination or abdominal and vaginal examinations to determine:
> Cervical effacement

> Cervical dilatation

> Descent of the fetal head through the maternal pelvis

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91
Q

What is inadequate uterine activity?

A

If contractions are inadequate the fetal head will not descend and exert force on the cervix and the cervix will not dilate.

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92
Q

How can the strength and duration of contractions be increased?

A

Giving a synthetic IV oxytocin to the mother

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93
Q

What is cephalopelvic disproportion (CPD)?

A

It means that the fetal head is in the correct position for labour but is too large to negotiate the maternal pelvis and be born!

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94
Q

Types of passage and passenger issues in labour?

A

> Cephalopelvic diproportion (CPD)
Malpresentation
Malposition

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95
Q

Which types of lie are there?

A

1) Longitudinal
2) Oblique
3) Transverse

They can then be:

1) Cephalic/vertex
2) Breeched
3) Shoulder presentation

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96
Q

What does cephalic or vertex presentation mean?

A

Head first

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97
Q

What does breech labour mean?

A

Feet first

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98
Q

What is malposition?

A

> Involves the fetal head being in an incorrect position for labour and ‘relative’ CPD occurs

> Occipito-posterior & Occipito-transverse

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99
Q

What can cause fatal distress?

A

Too many contractions (Uterine Hyper-stimulation) can result in fetal distress due to insufficient placental blood flow.

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100
Q

How is fatal well being determined?

A

Intermittent auscultation of the fetal heart:
> Cardiotocography
> Fetal blood sampling
> Fetal ECG

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101
Q

When is fatal blood sampling used?

A

When there is an abnormal CTG

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102
Q

What is being measured when using fatal blood sampling?

A

> We can measure pH and base excess

> pH gives a measure of likely hypoxaemia

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103
Q

Which situation are there in which labour is not advised?

A

1) Obstruction to birth canal
- Major placenta praevia, masses

2) Malpresentations
- Transverse, shoulder, hand, ??breech

3) Medical conditions where labour would not be safe for woman

4) Specific previous labour complications
- previous uterine rupture

5) Fetal conditions

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104
Q

What is the rate of assisted/ instrumental delivery?

A

Around 15% of births

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105
Q

What are the risks of caesarean section compared to vaginal birth?

A

1) Infection
2) Bleeding
3) Visceral injury
4) VTE

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106
Q

What are the benefits of Caesarean section?

A

Reduced risk of perineal injury compared with vaginal birth

107
Q

What s the average rate of caesarian section in the UK?

A

Around 25%

108
Q

What are the 3rd stage complications of labour?

A

> Retained placenta
Post partum haemorrhage
Tears

109
Q

What is the puerperium?

A

The postpartum period

110
Q

Post partum problems?

A

1) Bleeding
2) Infection (wound, endometritis, breast)
3) Problems with infant feeding
4) Problems with bonding
5) Social issues (partner, other children and financial issues)
6) Psychiatric issues

111
Q

Postnatal problems?

A

Post partum haemorrhage

Venous thromboembolism

Sepsis

Psychiatric disorders of the puerperium

Don’t forget pre-eclampsia

112
Q

How many times more likely is a pregnant woman to develop a thromboembolism (DVT or PE)?

A

6-10 times more likely

Immediately post part period there is still a state of hyper-coagulability

113
Q

What is the leading cause of maternal death in UK?

A

Sepsis

114
Q

If you suspect sepsis in any pregnancy woman what should you do?

A

1) Prompt IV antibiotic administration
2) Perform full septic screen = Blood cultures, LVS, MSSU, wound swabs
3) Antipyretic measures
4) IV fluids
5) Referral to hospital

115
Q

Almost a quarter of women who died between six weeks and one year after pregnancy died from what?

A

Mental-health related causes

116
Q

How to treat baby blues?

A

> Affects most women due to hormonal changes around the time of birth – usually 1-3 days PN

> Does not affect functioning and requires no specific treatment

117
Q

What is postnatal depression?

A

Postnatal Depression
> Can continue on from baby blues or start sometime later

> Has classical ‘depressive’ symptoms

> Affects functioning, bonding and often requires treatment

> Increased risk in women with personal or family history of affective disorder

118
Q

What is puerperal psychosis?

A

Puerperal psychosis:
> Rare but serious psychotic illness of the postnatal period

> Women can be a danger to themselves and their babies

> Requires inpatient psychiatric care

> Much more common in women with personal or family history of affective disorder, bipolar disorder or psychosis

119
Q

When do eclamptic seizures most commonly occur?

A

Most eclamptic seizures occur in the postnatal period

120
Q

What is spontaneous abortion or miscarriage?

A

The spontaneous termination of a pregnancy before 24 completed weeks gestation with no evidence of life

121
Q

What are the types of spontaneous miscarriage?

A 
> Threatened
> Inevitable
> Incomplete
> Complete
> Septic
> Missed
122
Q

What is the rate of spontaneous miscarriage?

A

Around 15% or higher

123
Q

What is a threatened miscarriage?

A

A threatened miscarriage refers to bleeding from the gravid uterus before 24 weeks gestation when there is a viable fetus and no evidence of cervical dilatation

124
Q

What is an inevitable miscarriage?

A

Abortion becomes inevitable if the cervix has already begun to dilate

125
Q

What is an incomplete miscarriage?

A

When there is only partial expulsion of the products of conception

126
Q

What is an complete miscarriage?

A

Complete expulsion of the products of conception is referred to as a complete abortion

127
Q

What is an septic miscarriage?

A

Following an incomplete abortion there is always a risk of ascending infection into the uterus which can spread throughout the pelvis and this is known as a septic abortion

128
Q

What is a missed miscarriage?

A

Missed abortion describes a pregnancy in which the fetus has died but the uterus has made no attempt to expel the products of conception.

129
Q

Signs/Symptoms of a threatened miscarriage?

Is this viable?

A

> Vaginal bleeding
+/- Pain
Closed cervix on speculum examination

This pregnancy is viable

130
Q

Signs/symptoms of a inevitable miscarriage?

Is this viable?

A

> Open cervix with bleeding, that could be heavy (+/- clots)

This pregnancy is viable

131
Q

Signs/symptoms of a missed miscarriage?

Is this viable?

A

> No symptoms

> Could have bleeding/ brown loss vaginally

> Gestational sac seen on scan

> No clear fetus (empty gestational sac) or a fetal pole with no fetal heart seen in the gestational sac

132
Q

Signs/symptoms of a incomplete miscarriage?

Is this viable?

A

> Open cervix, vaginal bleeding (may be heavy)

> Products of pregnancy may be seen within the uterus on US

133
Q

What type of miscarriage puts a woman at high risk of sepsis?

A

Incomplete miscarriage

134
Q

Aetiology of spontaneous miscarriage?

A

> Abnormal conceptus:

  - Chromosomal
  - Genetic, structural

> Uterine abnormality:

  - Congenital
  - Fibroids

> Cervical incompetence:

  - Primary
  - Secondary

> Maternal:

- Increasing age
- Diabetes

> Unknown

135
Q

What percentage of the population have a failure of normal fusion of the Mullerian ducts?

A

Approx 1%

Of these around 30% are likely to have spontaneous miscarriage

136
Q

How do you manage a threatened miscarriage?

A

Conservatively

137
Q

How do you manage a Inevitable miscarriage?

A

If bleeding heavy may require evacuation

138
Q

How do you manage a missed miscarriage?

A

> Conservatively

> Medical - Prostaglandins (misoprostol)

> Surgical - SMM (Surgical management of miscarriage)

139
Q

How do you manage a septic miscarriage?

A

Antibiotics and evacuate uterus

140
Q

What is an ectopic pregnancy?

A

Pregnancy implanted outside of the uterine cavity

141
Q

Where is the most common site of an ectopic pregnancy?

A

Tubal (95-97%):

1) Ampullary = Most common
2) Isthmus = Second most common

142
Q

What is the incidence of ectopic pregnancy?

A

1:90 pregnancies

143
Q

What are the risk factors of ectopic pregnancy?

A

> Pelvic inflammatory disease

> Previous tubal surgery

> Previous ectopic

> Assisted conception

144
Q

How would someone present with an ectopic pregnancy?

A

> Period of ammenorhoea (with +ve urine pregnancy test)

> +/- Vaginal bleeding
+/- Pain abdomen
+/- GI or urinary symptoms

145
Q

Which investigations would you perform for ectopic pregnancy?

A

Scan – no intrauterine gestational sac, may see adnexal mass, fluid in Pouch of Douglas

Serum BHCG levels – may need to serially track levels over 48 hour intervals- if a normal early intrauterine pregnancy HCG levels will increase by at least 66%ish

Serum Progesterone levels – with viable IU pregnancy high levels > 25ng/ml

146
Q

Which investigations would you perform for ectopic pregnancy - Scan?

A

Scan:
> No intrauterine
> Gestational sac
> May see adnexal mass, fluid in Pouch of Douglas

147
Q

Which investigations would you perform for ectopic pregnancy - Serum BHCG levels?

A

Serum BHCG levels – may need to serially track levels over 48 hour intervals- if a normal early intrauterine pregnancy HCG levels will increase by at least 66%ish

148
Q

Which investigations would you perform for ectopic pregnancy - Serum progesterone levels?

A

Serum Progesterone levels – with viable IU pregnancy high levels > 25ng/ml

149
Q

Management of ectopic pregnancy?

A

> Medical - Methotrexate

> Surgical (Mostly laparosciopical):

  • Salpingectomy
  • Salpingotomy for few indications

> Conservative

150
Q

Management of ectopic pregnancy - Medical?

A

Medical - Methotrexate

151
Q

Management of ectopic pregnancy - Surgical?

A

> Surgical (Mostly laparosciopical):

  • Salpingectomy
  • Salpingotomy for few indications
152
Q

What is antepartum haemorrhage?

A

APH - haemorrhage from the genital tract after the 24th week of pregnancy but before delivery of the baby.

APH is one of the gravest obstetric emergencies and is associated with significant maternal and neonatal morbidity and mortality.

153
Q

Causes of Antepartum Haemorrhage?

A

Placenta praevia

Placental abruption

APH of unknown origin

Local lesions of the genital tract

Vasa praevia (very rare)

154
Q

What is placenta praevia?

A

Placenta praevia is

where the placenta is attached to the lower segment of the uterus

155
Q

What is placental abruption?

A

Placental abruption is where the placenta has started to separate from the uterine wall before the birth of the baby and is associated with a retroplacental clot.

156
Q

What are some of the causes for APH?

A

> APH of unknown aetiology includes haemorrhage where other causes have been completely excluded.

> APH may be from local lesions within the genital tract including the cervix and the vaginal. For example cervical erosions and polps may cause an APH and occasionally cervical Ca may present with an APH whilst trichomonas or thrush infections within the vaginal can occasionallyt cause a blood stained discharge.

157
Q

What is Vasa praevia?

A

> All or part of the placenta implants in the lower uterine segment

> Vasa praeviua is a rare but serious cause of APH.

158
Q

What does Vasa praevia put someone at risk of?

A

> Usually the blood loss is small and is due to rupture of a fetal vessel within the fetal membranes. The blood loss is fetal and not maternal and the effect on the fetus can be catastrophic.

159
Q

What is the incidence of placenta praevia?

A

1/200 pregnancies

160
Q

What is the most common aetiology of placenta praevia?

A

> Multiparous women
Multiple pregnancies
Previous caesaren section

161
Q

How is placenta praevia graded?

A

Grade I = Placenta encroaching on the lower segment but not the internal cervical os

Grade II = Placenta reaches the internal os

Grade III = Placenta eccentrically covers the os

Grade IV = Central placenta praevia

162
Q

What is Grade I placenta praevia?

A

Grade I = Placenta encroaching on the lower segment but not the internal cervical os

163
Q

What is Grade II placenta praevia?

A

Grade II = Placenta reaches the internal os

164
Q

What is Grade III placenta praevia?

A

Grade III = Placenta eccentrically covers the os

165
Q

What is Grade IV placenta praevia?

A

Grade IV = Central placenta praevia

166
Q

How does placenta praevia present?

A

> Painless PV bleeding

> Malpresentation of the fetus

> Incidental

167
Q

Why does bleeding occur in placenta praevia?

A

With placenta preavia the bleeding is due to separation of the placenta as the lower uterine segment forms and the cervix effaces.

The blood loss occurs from the venous sinuses in the lower segment.

Usually the blood loss is painless and tends to be recurrent.

168
Q

How is placenta praevia diagnosed?

A

> Ultrasound is the first choice

> MRI scanning is more accurate method as it allows identification of the internal cervical os but is not widely available. Probably relevant if the USS is inconclusive.

169
Q

How is placenta praevia managed?

A

1) Patient is admitted to hospital
2) Vaginal examination is contraindicated
3) Diagnosis confirmed by US
4) Blood is cross matched and blood transfused depending on the maternal condition.
5) A conservative approach is adopted to prolong the pregnancy toi gain fetal maturity and then deliver by Caesareanb section.

There is a risk of PPH with PP.

170
Q

What must not be done in placenta praevia?

A

Vaginal examination should not be performed in placenta praevia

171
Q

Management of PPH?

A

1) Medical management – oxytocin, ergometrine, carbaprost, tranexemic acid
2) Balloon tamponade

3) Surgical:
- B Lynch cutre
- Ligation of uterine
- Iliac vessels
- Hystrectomy

172
Q

What is placental abruption?

A

Haemorrhage resulting from premature separation of the placenta before the birth of the baby and is associated with a retroplacental clot

173
Q

What is the incidence of placental abruption?

A

The incidence of placental abrution will depend on maternal age, parity and social status but it iu estimated to occur in approx 3% of all pregnancies

174
Q

Which factors are associated with placental abruption?

A

> Pre-eclampsia/ chronic hypertension

> Multiple pregnancy

> Polyhydramnios

> Smoking

> Increasing age

> Parity

> Previous abruption

> Cocaine use

175
Q

Types of placental abruption?

A

Placental abruption:

  • Revealed
  • Concealed
  • Mixed (concealed and revealed)
176
Q

Types of placental abruption - Revealed?

A

In revealed placental abruption the major haemorrhage is apparent externally because the blood released from the placenta escapes through the cervical os.

177
Q

Types of placental abruption - Concealed?

A

In concealed haemorrhage the haemorrhage occurs between the placenta and the uterine wall.

The uterine contents increase in volume and the fundal height is larger than would be consistent for gestation.

In some situations the blood penetrates the uterine wall and the uterus appears bruised and this is know as a Couvelaire uterus.

178
Q

Presentation of placental abruption?

A

> Pain

> Vaginal bleeding (may be minimal bleeding)

> Increased uterine activity (tone may be having contractions)

179
Q

General management of APH?

A

Management will vary from expectant treatment to attempting a vaginal delivery to immediate Caesarean section depending on:
1) Amount of bleeding

2) General condition of
mother and baby

3) Gestation

180
Q

Complications of placental abruption?

A

> Maternal shock, collapse (may be disproportionate to the amount of bleeding seen)

> Fetal death

> Maternal DIC, renal failure

> Postpartum haemorrhage - ‘couvelaire uterus’

181
Q

Preterm labour?

A

Onset of labour before 37 completed weeks gestation (259 days)

> 32-36 wks mildly preterm

> 28-32 wks very preterm

> 24-28 wks extremely preterm

It can be spontaneous or induced

182
Q

How common is preterm labour?

A

> Around 5-7% of singletons

> 30-40% within multiple pregnancies

183
Q

Predisposing factors for preterm labour?

A

> Multiple pregnancy

> Polyhydramnios

> APH

> Pre-eclampsia

> Infection eg UTI

> Prelabour premature rupture of membranes

> Majority no cause (idiopathic)

184
Q

How is preterm delivery diagnosed?

A

Contractions with evidence of cervical change on VE

185
Q

What should be consider within preterm labour?

A

The possible cause, e.g. abruption, infection etc

186
Q

Management Preterm Delivery - <24-26 weeks?

A

Generally regarded as very poor prognosis

decisions made in discussion with parents and neonatologists

187
Q

When are preterm deliveries considered viable?

A

After 26 weeks

188
Q

If a preterm labour is consider viable (>26 weeks) how should it be managed?

A

> Consider tocolysis to allow steroids/ transfer

> Steroids unless contraindicated

> Transfer to unit with NICU facilities

> Aim for vaginal delivery

189
Q

What is the major risk of preterm delivery?

A

Major cause of perinatal mortality and morbidity

This is gestation dependent

190
Q

What are the survival rates of preterm labours - <24 weeks?

A

6%

191
Q

What are the survival rates of preterm labours - 24 weeks?

A

26%

192
Q

What are the survival rates of preterm labours - 25 weeks?

A

43%

193
Q

What are the survival rates of preterm labours - 26 weeks?

A

48%

194
Q

What are the survival rates of preterm labours - 27 weeks?

A

73%

195
Q

What are the survival rates of preterm labours - 24 weeks?

A

84%

196
Q

What are the severe disability rates of preterm labours - <24 weeks?

A

65%

197
Q

What are the severe disability rates of preterm labours - 24 weeks?

A

38%

198
Q

What are the severe disability rates of preterm labours - 25 weeks?

A

31%

199
Q

What are the severe disability rates of preterm labours - 26 weeks?

A

26%

200
Q

Causes of neonatal morbidity in pretsrmurity?

A

1) Respiratory distress syndrome
2) Intraventricular haemorrhage

3) Cerebral palsy
nutrition

4) Temperature control
5) Jaundice
6) Infections
7) Visual impairment
8) Hearing loss

201
Q

Trophoblast cells of the fertilised egg (chorion) produce which hormone?

A

Trophoblast produces B-hCG or Beta-human Chorionic Gonadotrophi

202
Q

What is the target of B-hCG?

A

B-hCG – target is corpus luteum in ovary

203
Q

What is the function of B-hCG?

A

B-hCG – function is to stimulate corpus luteum to produce progestogen, which stops decidua from shedding

204
Q

Which hormone is used for the basis of pregnancy tests?

A

B-hCG

205
Q

What does the egg burrow into?

A

The decidua

206
Q

> Woman, 26 yrs
Misses period
Pregnancy test positive
Vaginal bleeding 7 weeks after missed period

What has probably happened? How is this confirmed

A

Miscarriage confirmed by US = No fetus present but membranes and decidua lining uterus still there

Decidual cast confirmed with removal of remaining tissue by obstetrician

207
Q

> Woman, 32 years old
Misses period.
8 weeks pregnant
Small amount of bleeding per vagina

Which tests should be performed?

A

> BhCG raised

> Ultrasound: Thickened lining of endometrial cavity. Expanded fallopian tube

Diagnosis = Ectopic pregnancy

Treatment = Considered using methotrexate – but opted for operative removal of fallopian tube  tissue sent to pathology

208
Q

Within ectopic pregnancy what predisposes to haemorrhage and rupture?

A

Lack of proper decidual layer and small size of tube predispose to haemorrhage and rupture

209
Q

> 32 year old woman
+ve pregnancy test
7 weeks pregnant – minor bleed

> Ultrasound: uterine cavity shows some placental tissue but no fetus. Fallopian tubes normal.
B-hCG raised

Diagnosis?

A

Miscarriage

Endometrial tissue removed by obstetrician and sent to pathology

Microscopy = enlarged abnormal chorionic villi with abundant trophoblast = molar pregnancy

210
Q

> Minor bleed

> Ultrasound: uterine cavity shows some placental tissue but no fetus. Fallopian tubes normal.

> B-hCG raised

> Microscopy = enlarged abnormal chorionic villi with abundant trophoblast

What is this?

A

A molar pregnancy

211
Q

How can a normal adult female switch off of certain genes in ova?

A

Mum to be switches off certain genes in ova (eggs) by methylating them

212
Q

How can a normal adult male switch off of certain genes in testes (sperm)?

A

Dad to be switches off different genes in sperm by methylating them

213
Q

What does the switching off of of certain genes in ova promote?

A

Promotes early baby growth

214
Q

What does the switching off of of certain genes in testes promote?

A

Dad’s changes promote early placenta growth via trophoblast proliferation

215
Q

What is the common cause of a molar pregnancy?

A

Various causes but often caused by 2 sperm fertilising one egg with no chromosomes

216
Q

In terms of genes what happens as a result of a molar pregnancy?

A

Empty ovum and 2 lots of dad’s genes with dads changes (methylation)

This results is imbalance in methylated (switched off) genes leading to trophoblast cells proliferate and therefore:

1) Overgrowth of placenta
2) All but no or all but non-existent fetal growth

because they have too many of dad’s methylated genes

217
Q

What can a molar pregnancy lead to?

A

A form of precancer of trophoblast cells

If it persists can (rarely) give rise to a malignant tumour called choriocarcinoma

218
Q

How to treat molar pregnancy?

A

1) Remove

2) If BhCG stays high (persistent disease) cure by methotrexate

219
Q

What is considered chronic hypertension in pregnancy?

A

Hypertension (>140/90 BP) either pre-pregnancy or at booking (≤ 20 weeks gestation)

220
Q

What is considered mild chronic hypertension in pregnancy?

A

Mild HT:
> Diastolic BP 90-99,
> Systolic BP 140-49

221
Q

What is considered moderate chronic hypertension in pregnancy?

A

Moderate HT:
> Diastolic BP 100-109
> Systolic BP 150-159

222
Q

What is considered severe chronic hypertension in pregnancy?

A

Severe HT:
> Diastolic BP ≥110
> Systolic BP ≥ 160

223
Q

What is gestational hypertension?

A

New hypertension (BP >140/90) after 20 weeks gestation

224
Q

What is pre-eclampsia?

A

New hypertension (BP >140/90) after 20 weeks gestation in association with significant proteinuria:

> Mild HT on two occasions more than 4 hours apart
Moderate to severe HT

+

> Proteinuria of more than 300 mgms/ 24 hours (protein urine
Protein:creatinine ratio > 30mgms/mmol)

225
Q

How can we test for significant proteinuria?

A

> Automated reagent strip urine protein estimation > 1+
Automated reagent strip urine protein estimation > 1+

> Spot Urinary Protein: Creatinine Ratio > 30 mg/mmol

> 24 hours urine protein collection > 300mg/ day

226
Q

What BP should be targeted for chronic hypertension in pregnancy?

A

<150/100 BP

227
Q

What is the pathophysiology of pre-eclampsia?

A

1) Immunological

2) Genetic predisposition:
- Secondary invasion of maternal spiral arterioles by trophoblasts impaired –> reduced placental perfusion

  • Imbalance between vasodilators / vasoconstrictors in pregnancy (prostocyclin / thromboxane)
228
Q

What are the risk factors for pre-eclampsia?

A

> First pregnancy

> Extremes of maternal age

> Pre-eclampsia in a previous pregnancy (esp. severe PET, delivery <34 weeks, IUGR baby, IUD, abruption)

> Pregnancy interval >10 years

> BMI > 35

> Family history of PET

> Multiple pregnancy

> Underlying medical disorders 
     - chronic hypertension
     - pre-existing renal disease
     - pre-existing diabetes
     - autoimmune disorders 
     – eg. antiphospholipid antibodies, SLE
229
Q

Maternal complications of pre-eclampsia?

A

Maternal:
- eclampsia - seizures

- severe hypertension – cerebral haemorrhage, stroke
 - HELLP (hemolysis, elevated liver enzymes, low platelets)
 - DIC (disseminated intravascular coagulation)
 - renal failure
 - pulmonary odema, cardiac failure
230
Q

Fetal complications of pre-eclampsia?

A

Impaired placental perfusion → IUGR, fetal distress, prematurity, increased PN mortality

231
Q

What are the symptoms/signs of severe PET?

A

> Headache, blurring of vision, epigastric pain, pain below ribs, vomiting, sudden swelling of hands face legs

> Severe Hypertension; > 3+ of urine proteinuria

> Clonus / brisk reflexes; papillodema, epigastric tenderness

> Reducing urine output

> Convulsions (Eclampsia)

232
Q

What are the biochemical abnormalities of severe PET?

A

> Raised liver enzymes
Bilirubin if HELLP present
Raised urea and urate
Creatinine

233
Q

What are the haematological abnormalities of severe PET?

A

> Low platelets
Low haemoglobin, signs of haemolysis
Features of DIC

234
Q

How do you monitor severe PET?

A

> Frequent BP checks, Urine protein

> Check symptomatology – headaches, epigastric pain, visual disturbances

> Check for hyper-reflexia (clonus), tenderness over the liver

> Blood investigations:

- Full Blood Count (for   hemolysis,  platelets) 
- Liver Function Tests 
- Renal Function Tests – serum urea, creatinine, urate
 - Coagulation tests if indicated

> Fetal investigations:

  • Scan for growth
  • Cardiotocography (CTG)
235
Q

What does PET stand for?

A

Pre-eclampsia toxaemia

236
Q

How is PET (Pre-eclampsia toxaemia) managed?

A

> Only ‘cure’ for PET is delivery of the baby and placenta

> Consider induction of labour / CS if maternal or fetal condition deteriorates, irrespective of gestation

> Conservative (aim for fetal maturity)

    - close observation of clinical signs &amp; investigations
    - anti-hypertensives (labetolol, methyldopa, nifedipine)
     - steroids for fetal lung maturity if  gestation  < 36wks

> Risks of PET may persist into the puerperium therefore monitoring must be continued post delivery

237
Q

How many pregnant woman suffer from PET?

A

5-8%

238
Q

How many pregnant woman suffer from severe PET?

A

0.5%

239
Q

How many pregnant woman suffer from eclampsia seizures?

A

0.05%

240
Q

What is the general ratio of eclampsia seizures in terms of being antepartum, intrapartum, postpartum?

A

1) Postpartum = 44%
2) Antepartum = 38%
3) Intrapartum = 18%

241
Q

What is the treatment for eclampsia seizures?

A

1) Magnesium sulphate bolus + IV infusion
2) Control of blood pressure – IV labetolol, hydrallazine (if > 160/110)
3) Avoid fluid overload – aim for 80mls/hour fluid intake

242
Q

Which prophylaxis is available for PET in subsequent pregnancies?

A

Low does Aspirin from 12 weeks till delivery

243
Q

What are women with PET at higher risk of developing in later life?

A

Hypertension

244
Q

What is gestational diabetes?

A

> Carbohydrate intolerance with onset (or first recognised) in pregnancy

> Abnormal glucose tolerance that reverts to normal after delivery

> However, more at risk of developing type II diabetes later in life

245
Q

If a woman has gestational diabetes what is she at higher risk of developing in the future?

A

Type II diabetes

246
Q

What happens to insulin requirements during pregnancy and why?

A

> Insulin requirements of the mother increase

> Because human placental lactogen, progesterone, human chorionic gonadotrophin and cortisol from the placenta have anti-insulin action

247
Q

Why does hyper-insulinemia occur?

A

If the mother is diabetic this leads to an increased glucose crossing the placenta and induces higher the normal production in the foetus leading to macrosomia.

Post-delivery this puts the neonate at higher risk of hypoglycaemia due to excess insulin production. Also increased risk of respiratory distress

248
Q

What does the effect of diabetes have on the foetus?

A

1) Fetal congenital abnormalities e.g – cardiac abnormalities, sacral agenesis (especially if blood sugars high peri-conception
2) Miscarriage
3) Fetal macrosomia, polyhydramnios
4) Operative delivery, shoulder dystocia
5) Stillbirth, increased perinatal mortality

249
Q

What does the effect of diabetes have on the mother?

A

1) Increased risk of pre-eclampsia
2) Worsening of maternal nephropathy, retinopathy, hypoglycaemia,
3) Reduced awareness of hypoglycaemia
4) Infections

250
Q

What does the effect of diabetes have on the neonates?

A

1) Impaired lung maturity
2) Neonatal hypoglycaemia
3) Jaundice

251
Q

Management of maternal diabetes preconception?

A

1) Better glycemic control, ideally blood sugars should be round 4 – 7 mmol/l pre-conception and HbA1c < 6.5% ( < 48 mmol/mol)
2) Folic acid 5mg
3) Dietary advice
4) Retinal and renal assessment

252
Q

Management of maternal diabetes during pregnancy?

A

1) Optimise glucose control – insulin requirements will increase:
< 5.3 mmol/l - Fasting
< 7.8 mmol/l - 1 hour postprandial
< 6.4 mmol/l - 2 hours postprandial
< 6 mmol/l – before bedtime

2) Could continue oral anti-diabetic agents (metformin) but may need to change to insulin for tighter glucose control
3) Should be aware of the risk of hypoglycaemia – provide glucagon injections/ conc. glucose solution
4) Watch for ketonuria/ infections
5) Repeat retinal assessments 28 and 34 weeks
6) Watch fetal growth
7) Observe for PET labour usually induced 38-40 weeks, earlier if fetal or maternal concerns
8) Consider elective caesarean section if significant fetal macrosomia
9) Maintain blood sugar in labour with insulin – dextrose insulin infusion

10 ) Continuous CTG fetal monitoring in labour

11) Early feeding of baby to reduce neonatal hypoglycemia
12) Can go back to pre-pregnancy regimen of insulin post delivery

253
Q

Risk factors for Gestational Diabetes Mellitus / consider screening for GDM?

A

1) Increased BMI >30
2) Previous macrosomic baby > 4.5kg
3) Previous GDM
4) Family history of diabetes
5) Women from high risk groups for developing diabetes – eg. Asian origin
6) Polyhydramnios or big baby in current pregnancy
7) Recurrent glycosuria in current pregnancy

254
Q

How do you screen for gestational diabetes mellitus?

A

> HbA1C:
1) if > 6% (43 mmol/mol), 75gms OGTT to be done.

2) If OGTT normal, repeat OGTT at 24 -28 weeks

Can also offer OGTT at around 16 weeks and repeat at 28 weeks if significant risk factors (eg. Previous GDM) present

255
Q

Management of gestational diabetes mellitus?

A

1) Control blood sugars – diet
2) Metformin/ insulin if sugars remain high
3) Post delivery – check OGTT 6 to 8 weeks PN
4) Yearly check on HbA1C/ blood sugars as at a higher risk of developing overt diabetes

256
Q

What is Virchow’s triad?

A

There element that lead to an increased risk of venous thromboembolism:

1) Stasis
2) Vessel wall injury
3) Hyper-coagulability

257
Q

What happens to the risk of throb-embolism during pregnancy and why?

A

> Risk of thrombo-embolism increased in pregnancy, due to being in a hyper coagulable state:

1) Increase in fibrinogen, factor VIII, VW factor, platelets
2) Decrease in natural anticoagulants – antithrombin III
3) Increase in fibrinolysis

> Increased stasis – progesterone, effects of enlarging uterus

> May be vascular damage at delivery/ caesearean section

Covering every aspect of Virchow’s triad

258
Q

What increases the risk even further of a thromboembolic-embolism during pregnancy?

A

> Older mothers, increasing parity

> Increased BMI, smokers

> IV drug users

> PET

> Dehydration – hyperemesis

> Decreased mobility

> Infections

> Operative delivery, prolonged labour

> Haemorrhage, blood loss > 2 l

> Previous VTE (not explained by other predisposing eg. fractures, injury), those with thrombophilia (protein C, protein S, Anti thrombin III deficiencies, etc), strong family history of VTE

> Sickle cell disease

259
Q

What prophylaxis is available for venous thrombosis-embolsim?

A

> TED stockings

> Advice increased mobility, hydration

> Prophylactic anti-coagulation with 3 or more risk factors (may be indicated even with one risk factor if significant risk), may need to continue 6 weeks postpartum

260
Q

Signs/ symptoms of VTE (Venous thrombosis-embolism)?

A

1) Pain in calf
2) Increased girth of affected leg

3) Calf muscle tenderness
breathlessness

4) Pain on breathing
5) Cough
6) Tachycardia
7) Hypoxic
8) Pleural rub, etc

261
Q

How should you investigate VTE (Venous thrombo-embolism)?

A 
> ECG
> Blood gases
> Doppler 
> V/Q (ventilation perfusion) lung scan 
> CTPA computed tomography pulmonary angiogram)

Appropriate treatment with anticoagulation
if VTE confirmed

262
Q

How should VTE be treated?

A

Venous thrombo-embolsim is treated with anticoagulation

263
Q

Do opiates cross the placenta? What occurs as a result? How would you manage?

A

1) Yes opiates cross the placenta
2) Pregnancy often proceeds well if mother eating properly
3) Immediate withdrawal from heroin when baby is born replace with methadone
4) Later withdrawal from methadone

264
Q

What is separation of placenta from the uterine wall?

A

Abruption, this leads to hypoxia in baby and often antepartum haemorrhage

If viable, emergency caesarian section should be performed

Year 3 - Reproduction (25 decks)

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