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Thick Stuff > Antenatal Obstetrics 2 > Flashcards

Antenatal Obstetrics 2 Flashcards

1
Q

Epidemiology of itchiness?

A

• Up to 25% of pregnancies

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2
Q

Aetiology of itchiness?

A

o May be liver related (gallstones, hepatits, HELLP) or pruritic eruption of pregnancy

o Generalised can be eczema, urticaria, scabies, etc

o Localised – candidiasis, pediculosis pubis

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3
Q

Symptoms/Signs of itchiness?

A

• PEP

o Intensely itchy papular/plaque rask on abdomen and limbs

o Common in first pregnancy beyond 35 weeks

o If vesicles, think pemphigoid gestationis

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4
Q

Investigations of itchiness?

A
  • Check for jaundice, problematic
  • Assess LFTs and bile salts
  • Urinalysis
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5
Q

Treatment of itchiness?

A
  • If liver pathology – get expert help promptly
  • PEP

o Emollients and weak topical steroids

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6
Q

Epidemiology of ankle oedema?

A

• Very common, almost normal

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7
Q

Symptoms/Signs of ankle oedema?

A

• Swelling, worse towards end of day

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8
Q

Investigations of ankle oedema?

A
  • BP
  • Urinalysis – protein
  • Check DVT
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9
Q

DDx of ankle oedema?

A

• Rule out pre-eclampsia

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10
Q

Treatment of ankle oedema?

A
  • Rest and leg elevation
  • Reassure harmless
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11
Q

Epidemiology, symptoms and treatment of leg cramps?

A
  • 30% affects, often latter half of pregnancy
  • Pain worse at night, can be severe
  • Raise foot of bed, pillows
  • Adequate Na and hydration
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12
Q

Epidemiology of nausea and vomiting in pregnancy?

A
  • Nausea = 80 – 85%
  • Vomiting = 52%
  • 20% persist after 20 weeks
  • Believed to be caused by hormones of pregnancy, especially hCG.
  • Can occur throughout the day
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13
Q

Symptoms and signs of nausea and vomiting in pregnancy?

A
  • Normally begins between 4th and 7th weeks gestation, peaks between 9th and 16th weeks and resolves around 20th week of pregnancy
  • Persistent vomiting and severe nausea can progress to hyperemesis gravidarum
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14
Q

Treatment of nausea and vomiting in pregnancy?

A
  • Frequent small meals
  • Reassure, encourage stress-free environment
  • Keep hydrated
  • May need antiemetics
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15
Q

Epidemiology, aetiology and symptoms of vaginitis?

A

• Common in pregnancy and often harder to treat

o Due to candidiasis

o Normal vaginal discharge may be heavier during pregnancy but need to exclude infection

• Itch, non-offensive white discharge associated with excoriations

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16
Q

Investigations and treatment of vaginitis?

A
  • Swabs can be taken
  • Imidazole vaginal pessaries
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17
Q

Epidemiology of hyperemesis gravidarum?

A

• Hyperemesis gravidarum is rare, with an incidence of 1/1000.

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18
Q

Pathology of hyperemesis gravidarum?

A
  • Defined as persistent vomiting in pregnancy which causes weight loss (>5% of pre-pregnancy weight) and ketosis
  • Thought to be due to high levels of hCG
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19
Q

Aetiology of hyperemesis gravidarum?

A

• Risk increased:

o Multiple pregnancies

o Molar pregnancies

o Previous HG

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20
Q

Symptoms and signs of hyperemesis gravidarum?

A
  • Inability to keep food or fluids down
  • Severe Vomiting
  • Weight loss
  • Dehydration
  • Hypovolaemia
  • Tachycardia
  • Electrolyte imbalance (low Na, low K, low B vitamins)
  • Haematemesis (Mallory-weiss tears)
  • Behavioural disorders
  • Ptyalism (inability to swallow)
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21
Q

Complications of hyperemesis gravidarum?

A
  • Maternal risks

 Liver and renal failure

 Hyponatraemia and rapid reversal of hyponatraemia leading to central pontine myelinosis.

 Thiamine deficiency may lead to Wernicke’s encephalopathy.

  • Fetal risks

 Intrauterine growth restriction (IUGR)

 Fetal death may ensure in cases with Wernicke’s encephalopathy

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22
Q

Investigations of hyperemesis gravidarum?

A
  • Urinalysis – detect for ketones in urine.
  • MSU to exclude UTI • FBC (high HCT)
  • U&E (Low K+, Na+, Metabolic hypochloraemic alkalosis)
  • LFT (high transaminases, low albumin)
  • Glucose
  • USS to exclude multiple and molar pregnancies and confirm viable intrauterine pregnancy
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23
Q

DDx of hyperemesis gravidarum?

A
  • Multiple pregnancy.
  • Molar pregnancy.
  • UTI
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24
Q

Initial treatment of severe hyperemesis gravidarum?

A
  • Admit if not tolerating oral fluid
  • NG feeds and reintroduce light diet slowly
  • IV fluids (NaCl or Hartmann’s)
  • VTE prophylaxis – enoxaparin SC, stockings
  • Psychological support required
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25
Q

Drug management of hyperemesis gravidarum? What about in severe?

A
  • Thiamine (thiamine hydrochloride 25-50mg PO TDS or thiamine 100mg IV infusion weekly)
  • Folic Acid 5mg/day
  • Antiemetics (regular or PRN) – Cyclizine, prochlorperazine, metoclopramide PO/IV/IM
  • Daily U&Es – replace Na and K+ if necessary.
  • Severe - prednisolone 40-50mg PO daily in divided doses or hydrocortisone 100mg/12h IV
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26
Q

Epidemiology of SFD?

A
  • 10% of babies are below the 10th centile.
  • 3% are below the 3rd centile for that gestation.
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27
Q

Definitions of SFD? What are the majority of SFD babies?

A

o Estimated foetal weight <10th centile for gestational age or abdominal circumference <10th centile

o Severe SFD - estimated foetal weight <3rd centile.

o The foetus is small for the expected size but continues to grow at a normal rate

o 50–70% of SGA fetuses are constitutionally small, with fetal growth appropriate for maternal size and ethnicity

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28
Q

Definitions of pre-term baby?

A

o Born before 37th week

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29
Q

Definition of IUGR? different types?

A

• IUGR – failure of growth in utero, may or may not result in baby being SGA

o Symmetrical – all growth parameters equally small, suggesting affected at early pregnancy, usually chromosomal abnormalities

o Asymmetrical – Weight centile < length and head circumference, usually due to IUGR and insult later in pregnancy

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30
Q

Complications of SFD?

A

o Risk of foetal death, congenital infections, hypoglycaemia, hypothermia, polycythaemia, NEC, meconium aspiration

o Higher incidence of cerebral palsy

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31
Q

Major risk factors for SFD?

A

 Age >40, smoker, cocaine, previous SGA/stillbirth, FHx SGA, hypertension, DM, renal impairment, pre-eclampsia

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32
Q

Minor risk factors for SFD?

A

 Nulliparity, BMI<20, IVF, PIH

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33
Q

Causes of IUGR?

A

o Poverty

o Constitutional

o Twins

o Infection, placental insufficiency (heart disease, hypertension, DM, smoking, sickle cell disease, pre-eclmpsia)

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34
Q

Symptoms and signs of SFD baby?

A
  • Identified on scans
  • <2.5kg baby, <10th centile for foetal age
  • Wrinkly, umbilical cord thin
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35
Q

Investigations for SFD/IUGR?

A

• Referral to consultant

o Foetal USS makes the diagnosis of SFD - measures head and abdominal circumferences

o Uterine artery Doppler if 3 or more risk factors and if abnormal, serial growth scans

o Foetal blood sampling or amniocentesis used to exclude chromosomal abnormalities

• BP and urinalysis – check for pre-eclampsia.

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36
Q

Diagnosing IUGR baby?

A

o Serial USS growth scans (2-3 weeks) and umbilical artery Doppler

o Monitoring weekly umbilical artery Doppler and daily CTG

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37
Q

Management of SFD?

A
  • Growth scans at fortnightly intervals.

o If Dopplers remain normal, no intervention but IOL at 37 weeks

o If Dopplers abnormal and preterm – delivery depends on ductus venosus Doppler

o If absent or reversed end-diastolic flow on Doppler – emergency LSCS

  • Corticosteroids for lung maturity up to 35+6 weeks
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38
Q

Labour management of IUGR?

A

o Transfer to centre with facilities for premature infants

o Ensure adequate resuscitation

o Take to NICU/SCBU

o May need supplemental milk if <2kg

o Tube or IV feeding

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39
Q

Post-birth management of SFD?

A

o Wrap up warm, encourage skin-to-skin contact

o Feed within 2h of birth

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40
Q

Outcomes of SFD?

A

o 90% of SGA catch up in first 2 years

o May be smaller as an adult

o Risk of CHD and obesity

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41
Q

Definition of LFD?

A

o Baby >90/95th centile in weight for gestation

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42
Q

Macrosomia definition?

A

o Excessive intrauterine growth beyond a specific threshold regardless of gestational age

o >4000/4500 g.

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43
Q

Causes of LFD?

A
  • Constitutionally large (usually familial)
  • Maternal diabetes (DM/GDM)
  • Obesity
  • Male sex
  • Multiparity
  • Weight gain during pregnancy
44
Q

Complications for LFD?

A

o Birth injury (shoulder dystocia perineal tearing, damage to coccyx)

o Hypoglycaemia

o Hypocalcaemia

o RDS

o Polycythaemia

o Jaundice

o Left-colon syndrome

45
Q

Labour complication in LFD?

A

• Shoulder dystocia may result in the collar bone being broken or in damage to the nerves in the shoulder and arm (brachial plexus).

46
Q

Investigations of LFD baby?

A
  • OGTT – to establish GDM
  • USS
  • CTG - in labour
47
Q

Management of LFD?

A
  • For most women, changing to a better position will help their babies be born without the need of an episiotomy (surgical cut to the perineum, which is the muscular area between the vagina and back passage) or other intervention.
  • Induction may be required especially if gestational diabetes.
48
Q

When does foetal movements start?

A
  • Start between 16 to 24 weeks gestation
  • Primigravida women will often not feel foetal movements until after 20 weeks gestation
49
Q

Pathology of reduced foetal movements?

A

• Reduced foetal movements are associated with stillbirth, fetal growth restriction, placental insufficiency, and congenital malformations

50
Q

Symptoms, treatment for reduced foetal movements?

A

Felt by mother or slowing or stopping of serial SFH

Lie on left side for 2 hours

If <26w - see community midwife

If >26w - MAU and CTG monitoring

51
Q

Epidemiology of prolonged pregnancy?

A
  • 5-10% of pregnancies
  • 30% if previous prolonged pregnancy
  • With a history of two this rises to 40%
52
Q

Definition of prolonged pregnancy?

A

o Pregnancy that exceeds >42 weeks gestation

o 294 days from the first day of the last menstrual period (LMP) in a woman with regular 28 day cycles.

53
Q

Aetiology of prolonged pregnancy?

A

• Dates cannot be relied upon in the following circumstances:

  • Uncertainty of LMP (10-30% of women).
  • Irregular periods.
  • Recent use of combined oral contraceptive pill (COCP)
  • Contraception during lactational amenorrhea.
54
Q

Foetal risks of prolonged pregnancy?

A
  • Intrapartum deaths are 4x more common.
  • Early neonatal deaths are 3x more common.
  • Meconium aspiration and assisted ventilation.
  • Oligohydramnios (too little amniotic fluid)
  • Macrosomia, shoulder dystocia and fetal injury.
  • Cephalohematoma
  • Fetal distress in labour.
  • Neonatal hypothermia, hypoglycaemia, polycythaemia and growth restriction.
55
Q

Maternal risks of prolonged pregnancy?

A
  • Maternal anxiety and psychological morbidity.
  • Increased intervention:

 Induction of labour.

 Operative delivery with ↑ risk of genital tract trauma.

56
Q

Signs of postmaturity in prolonged pregnancy?

A
  • Dry, cracked, peeling, loose skin
  • Decreased subcutaneous tissue, scaphoid abdomen, meconium staining nails and cord
57
Q

Investigations of prolonged pregnancy?

A
  • Confirm EDD
  • Discuss recommendation if spontaneous labour does not occur by 41 completed weeks, including membrane sweep and induction
  • Arrange visit at 41 weeks

Fetal monitoring:

  • Women should be offered daily CTGs (cardiotocography) after 42 weeks
58
Q

Management of prolonged pregnancy? Explain when and how

A

Offer membrane sweep – 41 weeks (+40 weeks in nullparity)

  • During an internal examination, sweep a finger around the cervix.
  • Thought to induce prostaglandins
  • May cause discomfort and little bleeding

Offer induction of labour between 41 and 42 weeks:

  • This slightly reduces perinatal mortality.
  • Done with vaginal prostaglandins followed by oxytocin
  • After induction – monitor foetus in labour (intermittent auscultation or continuous CTG)
59
Q

Management of prolonged pregnancy is woman declines induction?

A

o 2x weekly CTG and US estimation of amniotic fluid depth to detect hypoxic foetuses

o Doppler studies may be used o If CTG abnormal – consider LSCS

60
Q

How common is obstetric cholestasis?

A

Incidence 0.7%

61
Q

Symptoms of obstetric cholestasis?

A

Pruritus, especially palms and soles in second half of pregnancy, no rash and worse at night

62
Q

Diagnosis of obstetric cholestasis?

A

Diagnosis of exclusion Tests

  • LFTs, (transaminases and bilirubin raised) viral hepatitis, autoimmune screen, US of liver
63
Q

Risks to foetus of obstetric cholestasis?

A

Preterm labour, meconium and stillbirth

64
Q

Management of obstetric cholestasis?

A

Offer IOL at 37-38 weeks

Vitamin K if abnormal clotting screen to mother and baby

Ursodeoxycholic acid reduces pruritus

65
Q

Prognosis of obstetric cholestasis?

A

Symptoms resolves within days of pregnancy

Can recur with COCP and in subsequent pregnancies

66
Q

Epidemiology of PPROM?

A
  • Prematurity is leading cause of perinatal death and morbidity – 50% of perinatal deaths
  • 5-10% of births
  • Risk increases with number of births
67
Q

Define prematurity?

A
  • Premature – born <37 weeks gestation
68
Q

Causes of prematurity?

A

o Elective

o Multiple pregnancy

o APH, cervical incompetence, chorioamnionitis, uterine abnormalities, diabetes, polyhydramnios, pyelonephritis

o Idiopathic

69
Q

Risk Factors of prematurity?

A

o Previous preterm birth

o Multiple pregnancy

o Cervical surgery

o Uterine anomalies

o Pre-eclampsia

o IUGR

o Smoking

70
Q

Symptoms and signs of PPROM?

A
  • Popping sensation or gush with continuous watery liquid draining thereafter
  • Underwear may be damp
71
Q

Diagnosis of PPROM?

A
  • Seeing amniotic fluid draining from cervix and pooling in vagina after woman lying down for 30 mins
  • Sterile speculum examination – check for liquor and umbilical cord
  • If negative, IGF binding protein 1 or placental alpha-microglobin 1 test
72
Q

Management of PPROM?

A
  • Admit for 48h
  • Rule out evidence of chorioamnionitis and sepsis

o CRP, WBC, CTG

  • If chorioamnionitis – deliver asap
  • Monitor

o Temperature

o MSU

o HVS

73
Q

Drugs given in PPROM?

A
  • Corticosteroids (betamethasone) for lung maturity
  • Erythromycin 500mg PO QDS for 10 days (Alternative:penicillin)
  • 80% PPROM initiates labour
  • In 20% which don’t, if infection develops:

o Blood cultures

o IV Abx – Ampicillin + Gentamicin

o Labour asap

74
Q

Management of PPROM if labour does not occur?

A

o Discharge 48h, manage as out-patient

o Avoid intercourse, tampons and swimming

o Weekly follow-up in day unit – FBC and CRP done

o IOL after 34 weeks if cephalic

75
Q

Risk to foetus in PPROM?

A
  • Prematurity
  • Infection
  • Pulmonary hypoplasia
  • Limb contractures
76
Q

How common is multiple pregnancies? Twins/Triplets and Quadruplets?

A
  • 1 in 34 babies born in the UK is a twin or a triplet.
  • The incidence of multiple pregnancy has been rising but now appears to be stable at:
  • Twins = 3:200
  • Triplets = 1:5000
  • Quadruplets = 1:360,000

• Higher multiples than this are extremely rare but do occur.

77
Q

When does multiple pregnancy occur?

A
  • Multiple pregnancy occurs when two or more ova are fertilised to form dizygotic (non-identical) twins or a single fertilised egg divides to form monozygotic (identical) twins
78
Q

What is dizygotic twin?

A
  • Dizygotic multiple pregnancies, each foetus has its own placenta (either separate or fused), amnion and chorion
79
Q

What is monozygotic twin?

A
  • Monozygotic multiple pregnancies, the situation is more complex depending on the timing of the division of the ovum
80
Q

Describe types of monozygotic pregnancies depending on Day of division of ovum?

A

o Embryo splits at 3 days: dichorionic, diamniotic

o Embryo splits at 4-7 days: monochorionic, diamniotic

o Embryo splits at 8-12 days: monochorionic, monoamniotic

o Embryo splits at 13 days: conjoined twins (Siamese twins)

81
Q

What is twin-twin transfusion?

A
  • In monochorionic twin pregnancies, one twin can receive a reduced blood supply and have a slower growth rate (twin-twin transfusion)
82
Q

What happens in multiple pregnancies if one twin dies?

A
  • Sometimes, one fetus dies and forms a mummified fetus papyraceous or is reabsorbed
83
Q

Types of triplet pregnancies?

A

Triplet pregnancies can be monochorionic, dichorionic or trichorionic

84
Q

Risk factors for multiple pregnancies?

A
  • Previous multiple pregnancy.
  • Family history.
  • Increasing number of births.
  • Increasing maternal age.
  • Ethnicity (e.g. ↑Nigerians, ↓Japenese).
  • Assisted reproduction:
  • Clomiphene (10%)
  • Intrauterine insemination (IUI) (10-20%)
  • In vitro fertilisation (IVF) with two embryo transfer (20-30%).
85
Q

When is multiple pregnancy diagnosed?

A

• Diagnosed by USS in 1st trimester

86
Q

Early symptoms of multiple pregnancies?

A
  • Hyperemerisis gravidarum
  • Exaggerates other common symptoms
  • Uterus is larger than expected for dates – may be palpable earlier than 24 weeks
87
Q

Late symptoms of multiple pregnancies?

A
  • Large-for dates uterine size
  • Polyhydramnios
  • Higher than expected weight gain
  • More than two foetal poles may be palpable >24 weeks.
  • Two fetal hearts may be heard on auscultation
88
Q

Foetal complications of multiple pregnancies?

A

Stillbirth

Prematurity

Mortality

Feto-foetal transfusion syndrome (unequal blood distribution via MC placenta, MC monochorionic diamniotic twins)

IUGR

Congenital abnormalities (neural tube, cardiac, GI atresia)

Vanishing twin syndrome

89
Q

Maternal complications of multiple pregnancies?

A

iscarriage, anaemia, pre-eclampsia, haemorrhage, operative delivery, more severe symptoms of pregnancy, hyperemesis, GDM

90
Q

Labour complications of multiple pregnancies?

A

o Malpresentation

o Fetal hypoxia in second twin after delivery of the first.

o Cord prolapse

o Operative delivery

o Postpartum haemorrhage

o Rare: Cord entanglement (MCMA twins only), head entrapment with each other (‘locked twins’).

91
Q

Investigations in multiple pregnancies?

A

• USS – at dating scan majority

o Test for viability, chorionicity, nuchal translucency, malformation

• Monthly serial USS from 20 weeks (2 weekly if suggests TTTS)

92
Q

Antenatal management of multiple pregnancy?

A
  • Consultant-led care
  • Weekly antenatal clinics from 30 weeks
93
Q

Initial monitoring management of multiple birth at delivery?

A
  • Fe and Folic acid supplementation
  • IV access and anaesthetists at delivery
  • Continuous CTG
94
Q

When to offer delivery of multiple pregnancies?

A

• Offer elective birth at 37 weeks for uncomplicated dichorionic twins, 36 weeks for uncomplications monochorionic twins, 35 weeks for uncomplicated triplets

95
Q

Management of multiple pregnancies?

A
  • Steroids used if premature
  • 2nd twin is at increased risk of perinatal mortality – external cephalic version performed if needed
  • For vaginal delivery, the leading twin should be cephalic (~80% = head first) and there should be no absolute contraindications (e.g. two previous CS).
  • Triplets and higher order multiples are usually delivered by CS
  • Oxytocin can be used in labour and at delivery via infusion to present complications
  • One paediatrician per baby present
  • Post-natal support groups
96
Q

Two definitive US views of dichorionic pregnancy?

A
  • Obviously widely separated sacs or placentae = dichorionic
  • Membrane insertion showing the lambda sign = dichorionic
  • Fetuses of different sex = dichronionic (dizygotic)
97
Q

Diagnosis of monochorionic twins?

A

• Absence of the lambda sign <14 weeks diagnostic of monochorionic

98
Q

How can chorionicity be determined postnatally?

A

o Macroscopic and microscopic examination of membranes.

o Analysis of red blood cell markers.

o DNA probes

99
Q

What is leading cause of maternal death worldwide?

A

Haemorrhage

100
Q

Screening for infectious diseases - HIV

What happens if positive test?

A

MDT approach to optimise management through pregnancy

101
Q

Screening for infectious diseases - HepB

What happens if positive test? What is low/high risk?

A

Notifiable disease to HPA

Referred to hepatology

Women high viral load - antiretrovirals

All household contacts screening/vaccined, bottle feeding safer (can breast feed)

Low risk = (HepBe antibody +ve/Be antigen -ve)

High Risk = (HepBe antibody -ve/Be antigen +ve)

If high risk - newborn given immunoglobulins at birth

102
Q

Screening for infectious diseases - Syphilis

What happens if positive test?

A

Refer to GUM for Abx

Needs full treatment >4 weeks prior to delivery - if not newborn given IV therapy

Partner tracing

103
Q

Screening for infectious diseases - Rhesus negative

What happens if positive test?

A

All offered Anti-D immunoglobulin IV 28-30 weeks

IM Anti-D after delivery if baby Rh positive (cord blood sample taken at birth)

104
Q

Screening for infectious diseases - haemaglobinopathies

What happens if positive test?

A

Offered to all women

Family Origin Questionnaire identifies higher risk ethnic groups

If woman has trait, partner needs testing

105
Q

Management if baby is high risk of blood disorder (haemoglobinopathies)?

A

Prenatal diagnosis offered

Guthrie test identifies sickle cell disease

106
Q

What is not routinely screened for in booking visit?

A

HepC - unless IVDU, obstetric cholestasis

Chlamydia - encourage under 25s to participate in screening Group B strep

107
Q

Define DD, MD and MM twins? Which one is most at risk of TTFS?

A

Dichorionic–diamniotic—Twins who have their own chorions and amniotic sacs. They typically do not share a placenta and can be fraternal or identical.

Monochorionic–diamniotic—Twins who share a chorion but have separate amniotic sacs. They share a placenta and are identical.

Monochorionic–monoamniotic—Twins who share one chorion and one amniotic sac. They share a placenta and are identical.

TTFS = Monochorionic diamniotic twins

Thick Stuff (87 decks)

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