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Obs and Gynae > Obstetric Core Conditions > Flashcards

Obstetric Core Conditions Flashcards

1
Q

What is the lie of the fetus?

A

The lie describes the relationship of the fetus to the long axis of the uterus

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2
Q

What is the presentation of the fetus?

A

The presentation refers to the part of the fetus that occupies the lower segment of the uterus or the pelvis

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3
Q

What is abnormal lie?

A

When the fetus lie is either transverse or oblique (i.e. not parallel to the long axis of the uterus)

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4
Q

`What is normal lie?

A

When the fetus lie is longitudinal

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5
Q

What are the 2 types of fetal presentation in a longitudinal lie?

A

Cephalic and breech

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6
Q

What is the aetiology of abnormal lie?

A

Circumstances which allow more room to turn or conditions that prevent turning or prevent engagement

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7
Q

What conditions allow more room for the fetus to turn?

A 
Polyhydramnios
High parity (more lax uterus)
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8
Q

What conditions prevent the fetus turning?

A

Uterine or fetal abnormalities

Twin pregnancies

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9
Q

What conditions prevent engagement?

A

Placenta praevia
Pelvic tumours
Uterine deformities

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10
Q

__________ is more commonly complicated by an abnormal lie than labour at full term

A

Preterm labour

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11
Q

How common is abnormal lie?

A

1 in 200 births

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12
Q

What is the management for abnormal lie in a woman under 37 weeks pregnant who is not in labour?

A

No action required

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13
Q

What is the management for abnormal lie in a woman over 37 weeks pregnant?

A

Admit for US scan to identify a cause

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14
Q

After 37 weeks, a woman with abnormal lie is often admitted to hopsital in case the ______________ and an ultrasound scan is performed to exclude particular causes, notable __________ and __________.

A

Membranes rupture; polyhydramnios; placenta praevia

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15
Q

In the absence of pelvic obstruction, an abnormal lie will usually stabilise before how many weeks?

A

41 weeks

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16
Q

What is a breech presentation?

A

Presentation of the buttocks

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17
Q

How common is breech presentation?

A

Occurs in 3-4% of term pregnancies

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18
Q

What are the 3 types of breech presentation?

A

Extended (70%)
Flexed (15%)
Footling (15%)

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19
Q

What is the extended breech?

A

Both legs extended at the knee

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20
Q

What is the flexed breech?

A

Both legs flexed at the knee

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21
Q

What is the footling breech?

A

One or both feet present below the buttocks

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22
Q

What is the aetiology of a breech presentation?

A 
Idiopathic mostly
Previous breech presentation
Fetal and uterine abnormalities
Twin pregnancies
Placenta praevia 
Pelvic tumours
Pelvic deformities
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23
Q

Complications of abnormal lie

A

Labour cannot deliver fetus
Arm or umbilical cord prolapse when the membranes rupture
Uterine rupture if neglected

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24
Q

What is the management of abnormal lie after 41 weeks, if the pelvis is obstructed or if the woman is in labour?

A

Elective caesarean

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25
Q

__________ is commonly associated with breech presentation.

A

Prematurity

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26
Q

What are the complications of breech presentation?

A

Increased perinatal mortality and morbidity due to congenital anomalies (long term neurological handicap) and intrapartum problems (hypoxia and birth trauma)

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27
Q

How is a breech presentation managed?

A

After 37 weeks, external cephalic version (ECV) is attempted

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28
Q

What is the success rate of ECV?

A

50% success rate

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29
Q

Contraindications for ECV

A 
Antepartum haemorrhage
Ruptured membranes
Fetal compromise
Twins
Placenta praevia
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30
Q

What is the management of breech presentation if ECV has failed or is contraindicated?

A

Elective caesarean section slightly safer than a planned vaginal birth

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31
Q

Breech presentation is more common if __________ or a ___________

A

Preterm labour; previous breech presentation

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32
Q

What is the excess mortality in a breech presentation?

A

1%

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33
Q

What is an oblique fetal lie?

A

Head is in one iliac fossa

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34
Q

What is a transverse fetal lie?

A

Head is in the flank

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35
Q

Unstable lie in nulliparous women is ______ and usually signifies ________

A

Rare; obstruction

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36
Q

Why is ECV unjustified in managing an abnormal lie?

A

Fetus usually turns back

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37
Q

If ____________________________ occurs and persists for more than 48 hours, the mother is ________

A

Spontaneous cephalic version; discharged

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38
Q

Give an example of a uterine abnormality which could prevent fetal movement

A

Fibroids

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39
Q

Most common clinical feature of a breech presentation

A

Upper abdominal discomfort due to the hard head being palpable at the fundus

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40
Q

How is breech presentation diagnosis confirmed?

A

Ultrasound scan

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41
Q

What causes chicken pox?

A

Primary infection with herpes zoster virus

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42
Q

What is shingles?

A

Reactivation of a latent herpes zoster infection affecting adults in one or two dermatomes

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43
Q

How common is chicken pox in pregnancy?

A

0.03%

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44
Q

Chicken pox causes _____________________ in pregnancy

A

Severe maternal illness

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45
Q

How does a pregnant woman develop chicken pox?

A

If she is not immune to zoster, she can develop the infection after exposure to chicken pox or shingles

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46
Q

How common is teratogenicity in an early pregnancy chicken pox infection?

A

1-2%

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47
Q

Maternal infection in the 4 weeks preceding delivery can cause _____________

A

Severe neonatal infection

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48
Q

When is a severe neonatal chicken pox infection most common?

A

50% more common if delivery occurs within 5 days after or 2 days before maternal symptoms

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49
Q

How is a chicken pox infection treated during pregnancy?

A

Oral aciclovir

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50
Q

Pregnant women exposed to zoster are _____________

A

Tested for immunity

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51
Q

How is a chicken pox infection prevented in women who are non-immune?

A

IgG immunoglobulins given within 10 days of exposure

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52
Q

When are neonates given IgG immunoglobulins and closely monitored for chicken pox?

A

If neonate is delivered 5 days after or 2 days before maternal infection

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53
Q

How is chicken pox treated in a neonate?

A

Aciclovir

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54
Q

Infection is indicated in ___ of _____________ and is often ________

A

60%; preterm deliveries; subclinical

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55
Q

What is chorioamnionitis?

A

Infection of the fetus or placenta

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56
Q

Which bacteria is typically responsible for puerperal sepsis, and the most common bacterium associated with maternal death in the UK?

A

Group A streptococcus (Streptococcus pyogenes)

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57
Q

S. pyogenes is carried by how many people?

A

5-30%

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58
Q

What is the most common symptom of a S. pyogenes infection?

A

Sore throat

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59
Q

What are the clinical features of a S. pyogenes infection in pregnancy?

A

Chorioamnionitis with abdominal pain, diarrhoea and severe sepsis

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60
Q

What are the consequences of a S. pyogenes infection during pregnancy?

A

The fetus usually dies in utero and labour will then ensue

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61
Q

How is a S. pyogenes infection managed in pregnancy?

A

Early recognition, cultures and high dose antibiotics (and intensive care needed in severe cases)

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62
Q

How is S. pyogenes transmitted during pregnancy?

A

Maternal hand to perineal contamination (usually from children)

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63
Q

By what mechanism does chorioamnionitis cause preterm labour?

A

“The enemy knocks down the walls” (cervix is the wall)

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64
Q

What investigations should be done to identify chorioamnionitis?

A

Vaginal swabs - use sterile speculum if membranes ruptured
Maternal CRP raised
WCC raised on FBC (steroids also cause this to rise)
Lactate to assess severity of sepsis
CTG to asses fetal well-being

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65
Q

The presence of infection within the uterus is _____________ for the mother and _____________ for the neonate

A

Life threatening; worsens the outlook

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66
Q

How is chorioamnionitis treated?

A

IV antibiotics and immediate delivery, whatever the gestation

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67
Q

What are the clinical features of chorioamnionitis?

A 
Contractions/abdo pain
Fever/hypothermia
Tachycardia
Uterine tenderness
Coloured/offensive liquor
Fetal tachycardia
(clinical signs often appear late)
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68
Q

Normal BP changes in pregnancy

A

Falls to a minimum in the second trimester by about 30/15 mmHg (rises to pre-pregnant levels by term)

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69
Q

How are hypertensive disorders in pregnancy classified?

A

Pregnancy induced hypertension or pre-existing/chronic hypertension

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70
Q

2 types of pregnancy induced hypertension

A

Pre-eclampsia

Gestational hypertension

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71
Q

2 types of Pre-existing hypertension in pregnancy

A

Primary

Secondary

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72
Q

Why does BP normally fall in pregnancy?

A

Reduced vascular resistance

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73
Q

What determines BP?

A

Systemic vascular resistance and cardiac output

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74
Q

What is pre-existing hypertension in pregnancy?

A

Diagnosed when the BP is already treated or exceeds 140/90 mmHg before 20 weeks gestation

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75
Q

How common is underlying hypertension in pregnancy?

A

Occurs in 5% of pregnancies

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76
Q

Risk factors for pre-existing hypertension in pregnancy

A 
Old age
Obesity
Family history
Women who had hypertension after taking the COCP
Pregnancy induced hypertension
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77
Q

What is primary hypertension?

A

Idiopathic hypertension (most common)

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78
Q

What causes secondary hypertension?

A 
Obesity
Diabetes
Renal disease (polycystic disease, renal artery stenosis or chronic pyelonephritis)
Phaeochromocytoma
Cushing's syndrome
Cardiac disease
Coarctation of the aorta
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79
Q

Patients with underlying hypertension are at a sixfold increased risk of ___________________

A

Superimposed pre-eclampsia

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80
Q

What can cause pre-existing proteinuria during pregnancy?

A

Renal disease

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81
Q

Clinical features of pre-existing hypertension

A

BP increases in late pregnancy
Symptoms often absent
Proteinuria often present in patients with renal disease

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82
Q

What needs to be excluded when examining for pre-existing hypertension?

A

Fundal changes
Renal bruits
Radiofemoral delay

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83
Q

Complications of pre-existing hypertension

A

Worsening hypertension

Pre-eclampsia

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84
Q

Investigations for secondary hypertension

A

Two 24 hour urine collections for vanillylmandelic acid (VMA) to exclude phaeochromocytoma

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85
Q

What investigations need to be done for pre-existing hypertension?

A

Identify secondary hypertension
Look for coexistant disease
Identify pre-eclampsia

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86
Q

Investigations for co-existant disease with pre-existing hypertension

A

Renal function assessed

Renal ultrasound

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87
Q

How is pre-eclampsia identified?

A

Assess for proteinuria and uric acid levels and compare later in pregnancy with at booking

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88
Q

Why does phaeochromocytoma need to be exlcuded?

A

High maternal mortality

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89
Q

How is pre-existing hypertension managed during pregnancy?

A

Labetalol 1st line

Nifedpine 2nd line

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90
Q

Antihypertensives may not be required in the _____________ because of the _________________

A

2nd trimester; physiological fall in BP

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91
Q

Why are ACE inhibitors not used in pregnancy?

A

They are teratogenic and affect fetal urine production so must be changed before pregnancy

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92
Q

How is the risk of pre-eclampsia managed in pre-existing hypertension?

A

Lose dose aspirin
Screening using uterine artery doppler
Additional antenatal visits

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93
Q

What would indicate pre-eclampsia in a patient with pre-existing hypertension?

A

Worsening hypertension confirmed by significant proteinuria for the first time after 20 weeks

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94
Q

When is delivery usually undertaken in a patient with pre-existing hypertension?

A

38-40 weeks

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95
Q

What is a cord prolapse?

A

Occurs when, after the membranes have ruptured, the umbilical cord descends below the presenting part

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96
Q

What happens if a cord prolapse is untreated?

A

Cord is compressed or goes into spasm, and the baby becomes rapidly hypoxic

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97
Q

How often does cord prolapse occur?

A

1 in 500 deliveries

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98
Q

How is a cord prolapse diagnosed?

A

After identifying fetal distress, diagnosis made by a vaginal examination

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99
Q

Risk factors for a cord prolapse

A 
Preterm labour
Breech presentation
Polyhydramnios
Abnormal lie
Twin pregnancies
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100
Q

More than half of cord prolapses occur at _____________________

A

Artificial amniotomy

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101
Q

How is a cord prolapse managed initially?

A

The presenting part must be prevented from pressing the cord (either examining finger pushes it up or terbutaline is given)

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102
Q

What is terbutaline?

A

A tocolytic

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103
Q

If the cord is out of the introitus, it should be __________ but not __________

A

Kept warm and moist; forced back inside

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104
Q

What should the patient be doing whilst preparations are being made for delivering a baby with a cord prolapse?

A

Patient should be on all fours

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105
Q

How is a baby usually delivered with a cord prolapse?

A

Immediate caesarean section

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106
Q

How is a baby delivered with a cord prolapse if the cervix is fully dilated and the head is low?

A

Instrumental vaginal delivery

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107
Q

What is the fetal mortality of cord prolapse?

A

Rare if promptly treated

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108
Q

What is cytomegalovirus (CMV)?

A

A herpesvirus transmitted by personal contact

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109
Q

How many women in the UK are immune to CMV?

A

35%

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110
Q

Up to ___ of women develop CMV infection, usually ________ in pregnancy

A

1%; subclinical

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111
Q

CMV is a common cause of child ________ and _________

A

Handicap; deafness

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112
Q

How often is CMV vertically transmitted to the fetus?

A

40% of the time

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113
Q

What percentage of infected neonates are symptomatic at birth?

A

10%

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114
Q

What are the symptoms of CMV infection in neonates?

A 
IUGR
Pneumonia
Thrombocytopenia
Most develop severe neurological sequelae
Death
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115
Q

What severe neurological sequelae may a neonate develop if infected with CMV?

A

Hearing, visual and mental impairment

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116
Q

Asymptomatic neonates with CMV are at a ___ risk of _______

A

15%; deafness

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117
Q

Ultrasound abnormalities such as _________________ are evident in only ___ of CMV infections

A

Intracranial or hepatic calcification; 20%

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118
Q

How is a maternal CMV infection diagnosed?

A

Specifically requesting CMV testing
CMV IgM positive a long time after infection
Titres will rise
IgG avidity is low with recent infection

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119
Q

How is vertical transmission of CMV identified if maternal infection is confirmed?

A

Amniocentesis at least 6 weeks after maternal infection (and after 20+ weeks) will confirm or refute vertical transmission

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120
Q

How is CMV infection in pregnancy managed?

A

Close surveillance for US abnormalities to determine those at risk of neurological sequelae
No prenatal treatment
Termination offered

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121
Q

Why is routine screening for CMV infections not advised?

A

Most maternal infections do not result in neonatal sequelae and an amniocentesis involves risk

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122
Q

Is vaccination for CMV available?

A

No

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123
Q

Most neonates infected with CMV are ____________

A

Not seriously affected

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124
Q

Why does glucose tolerance decrease in pregnancy?

A

Altered carbohydrate metabolism and antagonistic effects of human placental lactogen, progesterone and cortisol

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125
Q

Why is pregnancy diabetogenic?

A

Women without diabetes but with impaired or potentially impaired glucose tolerance often deteriorate enough to classified as diabetic in pregnancy (gestational diabetes)

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126
Q

2 types of diabetes in pregnancy

A

Pre-existing, Type 1 (5%) or 2 (7.5%) or gestational diabetes (87.5%)

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127
Q

What percentage of pregnant women are affected by pre-existing diabetes?

A

1%

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128
Q

What are the maternal complications of pre-existing diabetes?

A 
Increased insulin requirements by 300%
Hypoglycaemia
Worsening retinopathy
Pre-eclampsia and hypertension
UTIs
Wound/endometrial infections after delivery
Operative/instrumental delivery more likely
Rarely ketoacidosis
Worsening IHD
Diabetic nephropathy
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129
Q

What are the fetal complications of pre-existing diabetes?

A

Congenital abnormalities (neural tube or cardiac defects)
Preterm labour
Reduced fetal lung maturity
Macrosomia (leads to polyhydramnios and increased urine output)
Birth trauma, shoulder dystocia
Fetal compromise, distress or death

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130
Q

Why is diabetes a problem in pregnancy?

A

Even slightly increased Glucose levels have adverse pregnancy effects

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131
Q

The kidneys of non-pregnant women start to excrete glucose at a threshold of _______

A

11mmol/L

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132
Q

Why is urinalysis for glycosuria not a useful diagnostic test for diabetes in pregnancy?

A

Kidneys excretion threshold for glucose decreases in pregnancy, so glycosuria may occur at physiological blood glucose concentrations

133
Q

What is macrosomia?

A

Excessive fetal growth

134
Q

What causes macrosomia?

A

Raised fetal blood glucose induce fetal pancreatic islet cell hyperplasia leading to hyperinsulinaemia which causes fat deposition and excessive growth

135
Q

What happens to insulin requirements in women with pre-existing diabetes during pregnancy?

A

Insulin requirements increase in order to maintain normoglycaemia

136
Q

Why are women with gestational diabetes less affected by diabetic complications in pregnancy?

A

Complications are related to glucose levels, and women with gestational diabetes generally have better control

137
Q

How is pre-existing diabetes managed?

A

Precise preconceptual glucose control
Fetal monitoring
Assessment of maternal complications
Consultant based antenatal care
Delivery in a unit with neonatal facilities
MDT approach (midwife, GP, obstetrician dietician)
Patient education

138
Q

Preconceptual management of pre-existing diabetes

A 
Optimal control of glucose levels
5mg folic acid given
Statins stopped
Antihypertensives substituted for labetalol or methyldopa
Assess renal function, BP and retinae
139
Q

What is optimal preconceptual glucose control?

A

Monthly HbA1c <48

Fasting glucose 4-7mmol/L

140
Q

What drugs can help optimise glucose levels?

A

Insulin and metformin

141
Q

How is renal function assessed?

A

Creatinine should be <120umol/L

142
Q

How are glucose levels managed during pregnancy?

A 
Metformin
Rapid acting insulin analogues
Doses progressively increased as pregnancy advances
Advice on exercise and diet
Glucagon
143
Q

How are glucose levels monitored during pregnancy, and what should they be?

A

HbA1c checked at booking
Home glucometer - fortnightly contact with healthcare professional
Fasting <5.3mmol/L
1 hour after food <7.8mmol/L

144
Q

How is insulin given for pre-existing diabetes in pregnancy?

A

Combination of once/twice daily long/intermediate acting with 3 preprandial short acting insulin injections
Fasting level should be >4mmol/L and glucagon is given

145
Q

How are the complications of pre-existing diabetes in pregnancy monitored?

A

Renal function checked
Retinae screened for retinopathy
(Repeated each trimester if any abnormal)

146
Q

How is the risk of pre-eclampsia in pre-existing diabetes managed?

A

75mg aspirin daily from 12 weeks

147
Q

How is diabetic ketoacidosis managed in pregnancy?

A

ABCDE emergency approach

148
Q

How is the fetus monitored if the mother has pre-existing diabetes?

A

Fetal echocardiography indicated

Growth scans at 32 and 36 weeks

149
Q

When is delivery advised for women with pre-existing diabetes?

A

37-39 weeks

150
Q

Elective caesarean is often used where the estimated fetal weight exceeds _____

A

4kg

151
Q

Why does the neonate commonly develop hypoglycaemia if the mother had pre-existing diabetes?

A

Fetus has become accustomed to hyperglycaemia and has high insulin levels

152
Q

What problems may arise in the neonate if the mother had pre-existing diabetes during her pregnancy?

A

Neonatal hypoglycaemia

Respiratory distress syndrome

153
Q

____________ is strongly advised in women with pre-existing diabetes

A

Breast feeding

154
Q

Neonatal blood glucose should be checked within _____ of birth

A

4 hours

155
Q

What can diabetic nephropathy lead to in pregnancy?

A

Massive proteinuria and deterioration in maternal renal function

156
Q

The mother’s dose of insulin can be ______________

A

Rapidly changed to pre-pregnancy levels after delivery

157
Q

What is eclampsia?

A

The occurrence of epileptiform (grand mal) seizures often as a drastic complication of pre-eclampsia

158
Q

Maternal complications of pre-eclampsia

A 
Eclampsia
Cerebrovascular haemorrhage
HELLP syndrome
Renal failure
Pulmonary oedema
159
Q

The occurrence of any complications of pre-eclampsia is an indication for __________

A

Delivery whatever the gestation

160
Q

How often does eclampsia occur?

A

0.03% of all pregnancies in UK

161
Q

What causes eclampsia?

A

Cerebrovascular vasospasm

162
Q

How does eclampsia cause mortality?

A

Hypoxia and concomitant complications of severe disease

163
Q

How is eclampsia treated?

A

Magnesium sulphate and intensive surveillance for other complications

164
Q

What are the causes of epileptiform seizures in pregnancy?

A

Maternal epilepsy
Eclampsia
Hypoxia from any cause

165
Q

Magnesium sulphate is not useful for ______________

A

Non-eclamptic seizures

166
Q

How are non-eclamptic seizures managed?

A

Airway cleared
O2 given
CPR if required
Diazepam normally stops seizure

167
Q

______________ is superior to ___________ in the eclamptic woman

A

Magnesium sulphate; diazepam

168
Q

Epilepsy affects ____ of pregnant women

A

0.5%

169
Q

Seizure control can deteriorate in _________, particularly in _______

A

Pregnancy; labour

170
Q

Why should antiepileptic treatment be continued during pregnancy?

A

Epilepsy is a significant cause of maternal death

171
Q

The risk of ___________ is increased by ____ in maternal epilepsy

A

Neural tube defects; 4%

172
Q

Why is the risk of congenital abnormalities such as NTDs increased in epilepsy?

A

Largely due to drug therapy

173
Q

What is the risk of a newborn having epilepsy if its mother has it?

A

3%

174
Q

The risks of NTDs in epilepsy are ____________, higher with ___________ and higher with certain drugs (e.g. __________)

A

Dose dependent; multiple drug usage; sodium valproate

175
Q

How is epilepsy managed in pregnancy?

A

Preconceptual assessment - swap to non-teratogenic drugs
Seizure control with as few drugs as possible at the lowest dose
5mg daily folic acid (high dose)

176
Q

Why should sodium valproate be avoided in pregnancy?

A

Associated with a higher rate of congenital abnormalities and with lower intelligence in children

177
Q

All women of reproductive age with epilepsy are best managed as if __________________________

A

They are contemplating pregnancy

178
Q

Which antiepileptics are safest in pregnancy?

A

Carbamazepine and lamotrigine

179
Q

__________ and __________ plasma levels fall in pregnancy so __________ are commonly required

A

Lamotrigine; levetiracetam; dose increases

180
Q

From 36 weeks, _____________ is given orally for women on enzyme inducing antieplipetics

A

10mg Vitamin K

181
Q

How are fetal abnormalities excluded in epileptic women?

A

20 week scan and fetal echocardiography

182
Q

What is slow labour?

A

Progress slower than 0.5cm/hour after 4cm (the latent phase)

183
Q

What is prolonged labour?

A

> 12 hour duration after the latent phase

184
Q

Slow progress in labour is common in ___________ bur rare in _____________

A

Nulliparous women; multiparous women

185
Q

How does the ‘powers’ contribute to slow progress in labour?

A

Inefficient uterine action

186
Q

How does the ‘passenger’ contribute to slow progress in labour?

A

Fetal size
Disorders of rotation
Disorders of flexion

187
Q

Disorders of rotation

A

Occipito-transverse position

Occipito-posterior position

188
Q

Disorder of flexion

A

Brow presentation

Face presentation

189
Q

How does the ‘passage’ contribute to slow progress in labour?

A

Cephalo-pelvic disproportion

Rarely cervical resistance

190
Q

General management for slow progress in labour

A

Wait if natural labour is wanted
Mobilise
Improve support

191
Q

Management for slow progress in labour for nulliparous women

A

Amniotomy

Oxytocin

192
Q

Management for slow progress in labour for multiparous women

A

Amniotomy

Oxytocin if malpresentation/malposition excluded

193
Q

What is the management for slow progress in the first stage of labour if all else fails?

A

Caesarean section

194
Q

What is the management for slow progress in the second stage of labour if all else fails?

A

Instrumental delivery

195
Q

What is fetal distress?

A

An acute situation such as hypoxia that may result in fetal damage or death if it is not reversed or if the fetus is delivered urgently

196
Q

What is occipito-posterior position?

A

Abnormality of rotation, with the face upwards (some extension is common)

197
Q

How often does the OP position occur?

A

5% of deliveries

198
Q

When is OP position more common?

A

Early labour

199
Q

What is the aetiology of the OP position?

A

Idiopathic
Inefficient uterine action
Pelvic variants

200
Q

What are the features of OP position?

A

Slow labour
Back pain
Early desire to push
Occiput posterior on vaginal examination

201
Q

Management of OP position if progress is normal

A

Nil

202
Q

Management of OP position if slow progress

A

Amniotomy and oxytocin (cautious if multiparous)
C-section if these fail in 1st stage
Rotational instrumental delivery if these fail in 2nd stage (and >1-2h of pushing)

203
Q

Causes of permanent fetal damage attributable to labour

A 
Fetal distress/hypoxia
Infection e.g. group B strep
Meconium aspiration leading to chemical pneumonitis
Trauma e.g. forceps
Fetal blood loss
204
Q

____ of cerebral palsy cases are attributed solely to intrapartum problems

A

10%

205
Q

What indicates significant fetal hypoxia?

A

pH of <7.20 in fetal scalp (capillary) blood or ominous fetal heart rate abnormalities

206
Q

At what fetal capillary pH is neurological damage considerably more common?

A

<7.00

207
Q

What is the aetiology of fetal distress?

A

Contractions temporarily reduce placental perfusion and may compress the umbilical cord
So longer labours and excessive time spent pushing (>1 hour) more likely to produce hypoxia

208
Q

What can cause acute hypoxia in labour?

A 
Placental abruption
Hypertonic uterine states
Oxytocin
Prolapse of umbilical cord
Maternal hypotension
209
Q

Intrapartum risk factors for fetal distress

A

Long labour
Meconium
Epidural or oxytocin use
Maternal fever

210
Q

Antepartum risk factors for fetal distress

A

Pre-eclampsia
Diabetes
IUGR

211
Q

Fetuses with risk factors for fetal distress are usually ________________________

A

Monitored in labour with CTG

212
Q

How is fetal distress diagnosed/detected?

A 
Colour of the liquor - meconium
Fetal HR auscultation
Cardiotocography (CTG)
Fetal ECG
Fetal blood (scalp) sampling
213
Q

Level 1 screening for fetal distress

A

Intermittent auscultation of fetal heart. If it is abnormal, or meconium inspected, or a long or high risk labour proceed to level 2

214
Q

Level 2 screening for fetal dstress

A

Continuous CTG. If sustained bradycardia >5min, deliver.

If abnormal on other criteria, proceed to level 3.

215
Q

Level 3 screening for fetal distress

A

Fetal blood sampling. If abnormal proceed to level 4

216
Q

Level 4 screening for fetal distress

A

Delivery by quickest route (C-section if 1st stage, Instrumental vaginal if 2nd stage)

217
Q

Normal features of a CTG

A

Rate 110-160
Accelerations
Variability >5bpm

218
Q

Abnormal features of a CTG

A

Tachy or bradycardias
Decelerations
Reduced variability

219
Q

Indications for a CTG

A

Prelabour risk factors - pre-eclampsia, IUGR, previous C-section, induction
In labour risk factors - meconium, oxytocin use, temp >38C, during epidural analgesia
Intermittent auscultation abnormalities

220
Q

Management of fetal distress

A

In utero resuscitation

If this fails, fetal blood sampling (delivery if pH <7.20)

221
Q

How is in utero resuscitation performed?

A 
Place woman in left lateral position to avoid aortocaval compression
O2 and IV fluids given
Oxytocin stopped
Stop contractions using terbutaline
Vaginal exam to exclude cord prolapse
222
Q

Mechanism of action of terbutaline

A

Beta 2 agonist

223
Q

When is immediate delivery expedited?

A

FBS pH <7.20

CTG shows sustained bradycardia

224
Q

What is small for gestational age (SGA)?

A

The weight of the fetus is less than the tenth centile for its gestation (2.7kg at term)

225
Q

What is intrauterine growth restriction (IUGR)?

A

Fetus is small compared to its genetic potential and is compromised

226
Q

Aetiology of SGA

A

Asian ethnicity
Nulliparity
Female fetal gender
Low maternal weight and height

227
Q

Aetiology of IUGR

A 
Maternal illness (renal disease, pre-eclampsia)
Multiple pregnancy
Chromosomal abnormalities
Infections (CMV)
Smoking, drug use
Malnutrition
228
Q

Clinical features of IUGR

A

Low symphysis-fundal height

Features of pre-eclampsia (check BP and urine for proteinuria)

229
Q

How is SGA/IUGR invetsigated?

A

US scan
Fetal anomaly scan
Check CMV status
Chromosomal abnormalities via amniocentesis
Umbilical artery doppler (umbA) if <34 weeks
UmbA and middle cerebral artery doppler (for cerebroplacental ratio) if >34 weeks
CTG if dopplers severely abnormal (e.g. AEDF)

230
Q

Management of SGA <37 weeks

A

Monitor growth with US every 2-3 weeks

231
Q

Management of SGA >37 weeks

A

No intervention if growth is consistent and umbA normal

Consider delivery

232
Q

Management of IUGR <34 weeks

A

Twice weekly umbA doppler if they are abnormal (but no absent end diastolic flow - AEDF)
Admission and steroids if AEDF
Daily CTG if AEDF <32 weeks
Deliver by C-section if umbA shows AEDF >32 weeks or if CTG abnormal
Give magnesium sulphate just prior to delivery

233
Q

Management of IUGR >34 weeks

A

Monitor CPR
Consider delivery
Induce delivery by 37 weeks

234
Q

What is fetal compromise?

A

A chronic situation when conditions for the normal growth and neurological development are not optimal, commonly causing IUGR

235
Q

Causes of fetal compromise

A

Poor nutrient transfer via the placenta (placental dysfunction)

236
Q

IUGR is a major cause of ________

A

Stillbirth

237
Q

Complications of IUGR

A 
Stillbirth
Fetal distress in labour
Neonatal unit admission
Long term handicap
Preterm delivery
Maternal risks (due to pre-eclampsia or caesarean)
238
Q

Why is reduced fetal movements not a consistent feature of IUGR?

A

A compromised fetus only stops moving when very unwell

239
Q

_________ commonly co-exists with IUGR

A

Pre-eclampsia

240
Q

Major risk factors for SGA at booking

A 
Previous SGA or stillbirth
Heavy smoking
Cocaine use
Heavy daily exercise
Diabetes or other maternal illness
Parental SGA
241
Q

A reduction in ___________ by 30% of the _______________ suggests IUGR

A

Growth velocity; abdominal cirucmference

242
Q

What is oligohydramnios?

A

Reduced volume of amniotic fluid (sign of IUGR)

243
Q

CTG becomes abnormal in IUGR only when _____________________

A

Severe compromise of fetal distress is present

244
Q

What is gestational diabetes?

A

Carbohydrate intolerance diagnosed in pregnancy which may or may not resolve after pregnancy, causing glucose levels to rise temporarily to diabetic levels

245
Q

Why is gestational diabetes becoming more common?

A

Increasing prevalence of obesity

246
Q

What proportion of pregnant women develop gestational diabetes?

A

16%

247
Q

How is gestational diabetes diagnosed?

A

Fasting glucose >5.6mmol/L

Abnormal glucose tolerance test (GTT)

248
Q

What is an abnormal glucose tolerance test?

A

Glucose >7.8mmol 2 hours after a 75g glucose load

249
Q

Risk factors for gestational diabetes

A 
Previous gestational diabetes
Previous fetus >4.5kg
Previous unexplained stillbirth
First degree relative with diabetes
BMI >30
South Asian, black Caribbean or Middle Eastern
Polyhydramnios
Persistent glycosuria
250
Q

Risk based screening for gestational diabetes

A

GTT at 28 weeks if risk factors present

251
Q

When is the GTT performed in women with previous gestational diabetes?

A

18 weeks

252
Q

Initial treatment for gestational diabetes

A

Give glucometer
Advise diet and exercise
Check HbA1c for pre-existing diabetes
If fasting >7, treat with insulin as pre-existing diabetic
If fasting <7 but after 2 weeks levels >5.3 before meals or >7.8 1 hour after meals, treat with metformin

253
Q

Antenatal care for gestational diabetes

A

Managed as for pre-existing diabetes

If well controlled, delivery need not be before 41 weeks (induce at this point)

254
Q

A fasting glucose should be measured _________ postpartum in women with gestational diabetes

A

6 weeks

255
Q

More than ____ of women with gestational diabetes will become diabetic within the next 10 years

A

50%

256
Q

What is gestational hypertension?

A

New hypertension after 20 weeks without proteinuria

257
Q

Management for gestational hypertension

A

Monitor for fetal compromise

Delivery by 40 weeks is usual

258
Q

What criteria make up HELLP syndrome?

A

Haemolysis
Elevated Liver enzymes
Low platelets

259
Q

Clinical features of haemolysis

A

Dark urine
Raised lactic dehydrogenase (LDH)
Anaemia

260
Q

Clinical features of elevated liver enzymes

A

Epigastric pain
Liver failure
Abnormal clotting

261
Q

Low platelets in HELLP syndrome is normally ___________

A

Self limiting

262
Q

What is HELLP syndrome?

A

Liver and coagulation problems occurring as a complication of pre-eclampsia

263
Q

What other features may occur with HELLP syndrome?

A

DIC
Liver failure
Liver rupture
Liver infarction or subcapsular haemorrhage

264
Q

Treatment of HELLP syndrome

A

Supportive
Magnesium sulphate prophylaxis against eclampsia
Intensive care in severe cases

265
Q

Investigations to diagnose HELLP syndrome

A

Rapid fall in platelets
Rise in LFTs (ALT) - liver damage
LDH levels rise
Rising creatinine (impaired renal function)

266
Q

What causes a rapid fall in platelets in HELLP syndrome?

A

Platelet aggregation on damaged endothelium

267
Q

What is induction of labour?

A

Labour started artificially

268
Q

What is augmentation?

A

When contractions of established labour are strengthened

269
Q

When is induction of labour performed?

A

Situations where allowing the pregnancy to continue would expose the fetus and/or the mother to risk greater than that of induction

270
Q

What determines the whether or not induction is successful?

A

The state or favourability of the cervix

271
Q

The lower the Bishop’s score, the more ______________ the cervix is for induction

A

Unfavourable

272
Q

How is the state of the cervix measured?

A

Bishop’s score or transvaginal ultrasound

273
Q

What components make up Bishop’s score?

A 
Consistency of cervix
Degree of effacement of cervix
Cervical dilatation
Station of the head
Cervical position (anterior or posterior)
274
Q

What is the station of the fetal head?

A

How low in the pelvis the fetal head is

275
Q

Medical methods of induction

A

Prostaglandin E2

Oxytocin (after amniotomy/membrane rupture)

276
Q

Surgical methods of induction

A

Amniotomy

277
Q

How is PGE2 used to induce labour?

A

Gel or slow release preparation is inserted into the posterior vaginal fornix

278
Q

When is PGE2 best used for induction?

A

Nulliparous women

Most multiparous women (unless cervix is very favourable)

279
Q

PGE2 either __________ or improves the _____________ to allow amniotomy

A

Starts labour; ‘ripeness’ of the cervix

280
Q

How is amniotomy and oxytocin used to induce labour?

A

Forewaters are ruptured using an amnihook to artificially rupture membranes
Oxytocin infusion given within 2 hours if labour has not ensued

281
Q

When is oxytocin used alone to induce labour?

A

If spontaneous rupture of the membranes has already occured

282
Q

What is natural induction?

A

Cervical sweeping involves passing a finger through the cervix and ‘stripping’ between the membranes and the lower segment of the uterus

283
Q

At 40 weeks, natural induction reduces the chance of __________ and ______________

A

Induction; postdates pregnancy

284
Q

Fetal indications for induction of labour

A 
Prolonged pregnancy
Suspected IUGR or compromise
Antepartum haemorrhage
Poor obstetric history
Prelabour term rupture of membranes
285
Q

Materno-fetal indications for induction of labour

A

Pre-eclampsia

Diabetes or hypertension

286
Q

Maternal indications for induction of labour

A

Social reasons

In utero death

287
Q

Absolute contraindications for induction of labour

A 
Acute fetal compromise (abnormal CTG)
Abnormal lie
Placenta praevia
Pelvic obstruction (mass or deformity)
Cephalo-pelvic disproportion
288
Q

Relative contraindications for induction of abour

A

One previous caesarean section (scar rupture)

Prematurity

289
Q

Why is the fetus at an increased risk during induced labour?

A

Use of drugs

Indication for induction

290
Q

How is induced labour managed?

A

CTG monitoring

Oxytocin needed in labour

291
Q

Induction commonly increases the __________________

A

Time spent in early labour

292
Q

Complications of induced labour

A 
Inefficient uterine activity
Hyperstimulation
Postpartum haemorrhage
Intra/postpartum infection
Prematurity
Risk of instrumental delivery or caesarean
293
Q

What is the consequence of inefficient uterine activity when inducing labour?

A

Labour may fail to start or be slow

294
Q

What are the consequences of hyperstimulation when inducing labour?

A

Fetal distress

Uterine rupture

295
Q

What is the incidence of twins?

A

1.3%

296
Q

What is the incidence of triplets?

A

0.1%

297
Q

The incidence of twins is increasing due to _____________ and ____________

A

Fertility treatments; older mothers

298
Q

What are dizygotic twins?

A

Different oocytes fertilized by different sperm

299
Q

What are monozygotic twins?

A

Division of the zygote after fertilization by one sperm

300
Q

What are dichorionic twins?

A

Two placentas and two amniotic sacs (can be dizygotic or monozygotic)

301
Q

What are monochorionic twins?

A

Shared placenta (always monozygotic)

302
Q

What proportion of twins are dichorionic?

A

70%

303
Q

What are monochorionic diamniotic twins?

A

Identical twins (MZ) that share a placenta but not amniotic sac

304
Q

What proportion of twins are monochorionic diamniotic?

A

30%

305
Q

What are monochorionic monoamniotic twins?

A

Identical twins (MZ) that share a placenta and amniotic sac

306
Q

What proportion of twins are monochorionic monoamniotic?

A

1%

307
Q

Aetiology of multiple pregnancies

A

Ovulation induction and IVF
Genetic factors
Increasing age and parity

308
Q

How are multiple pregnancies diagnosed?

A

US scan
Vomiting
Large for dates
More than 3 fetal poles

309
Q

Maternal complications of multiple pregnancies

A

Pre-eclampsia
Anaemia
Gestational diabetes
Operative delivery

310
Q

Fetal complications of multiple pregnancies

A 
Increased morbidity and mortality
Miscarriage
Preterm labour
Placental insufficiency
IUGR
Ante/postpartum haemorrhage
Malpresentations
311
Q

Fetal complications for monochorionic twins

A

Congenital abnormalities
Twin-twin transfusion (TTTS)
IUGR

312
Q

Management for women with multiple pregnancies

A 
Early diagnosis
Identification of chorionicity
Consultant care
Iron and folic acid supplements
Anomaly scan
Surveillance for pre-eclampsia, diabetes, anaemia
Serial US at 28, 32 and 36 weeks
313
Q

Management for women with monochorionic twins

A

US fortnightly from 12 weeks for TTTS and IUGR

314
Q

When are dichorionic twins delivered?

A

37 weeks

315
Q

When are monochorionic twins delivered?

A

36 weeks

316
Q

When is a caesarean indicated for twins?

A

If first twin is not cephalic

317
Q

What monitoring is needed whilst delivering twins?

A

CTG

318
Q

How is the second twin delivered?

A

Lie of second twin checked
ECV to longitudinal lie if necessary
Amniotomy when presenting part s engaged, then maternal pushing

319
Q

When is a ventouse or breech extraction necessary for delivering twins?

A

If fetal distress

320
Q

What is the incidence of twin-twin transfusion syndrome (TTTS)?

A

15% of all monochorionic twins

321
Q

What is the pathology of TTTS?

A

Unequal blood distribution in a shared placenta leading to discordant blood volumes, liquor and growth

322
Q

How is TTTS diagnosed?

A

Discordant liquor volumes

323
Q

Clinical features of the recipient twin in TTTS

A

Larger twin
Polyhydramnios
Fluid overload
Heart failure

324
Q

Clinical features of the donor twin in TTTS

A

Smaller twin

Oligohydramnios

325
Q

Complications of TTTS

A

Late miscarriage
Severe preterm delivery
In utero death
Neurological damage

326
Q

How is TTTS managed?

A

US surveillance from 12 weeks

Laser ablation if TTTS is diagnosed

327
Q

What is the prognosis of untreated TTTS?

A

Very poor if untreated

328
Q

What is the prognosis of TTTS with laser ablation?

A

50% both twins survive

80% one twin survives

Obs and Gynae (2 decks)

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