Antenatal Care Flashcards

1
Q

What are the main principles of antenatal care?

A

Education on normal physiological changes
Identify maternal risk factors early
Screen & diagnose maternal disease,
Screen & diagnose fetal problems.

Birth plan, postnatal care & parenting, next pregnancy

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2
Q

What is the antenatal schedule for uncomplicated and high risk pregnancies?

A

Low risk (uncomplicated pregnancy) = midwife only.

  • Booking by 10 weeks
  • 10 appointments for nulliparous
  • 7 appointments for multiparous

High risk = doctor & midwife
- referral to consultant led care (at booking or later when develops risk factors), continue with care in community as appropriate, deliver in high risk maternity units but risk assess.

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3
Q

What aspects of antenatal care are carried out preconception?

A

Folic acid 3 months prior
Avoid teratogens
Counselling: lifestyle (smoking, alcohol, weight), optimise medical disorders, ideal timing (age related risk).

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4
Q

When pregnant, what should be done at first contact with health care professional? (NICE, 2008)

A

Folic acid, food hygiene, lifestyle advice, all antenatal screening including haemoglobinopathies, anomaly scan & Down’s syndrome screening (include risks & benefits of screening).

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5
Q

What information should be given at booking (8-10 weeks)?

36 weeks?

38 weeks?

A

Booking (ideally by 10 weeks):

how baby develops, nutrition/diet including vitamin D supplementation & the Healthy Start program, exercise (including pelvic floor exercises), place of birth, pregnancy care pathway, breastfeeding (including workshops), participant-led antenatal classes, further discussion of all antenatal screening, discussion of mental health issues

Before or at 36 weeks: breastfeeding info (technique, good management practices), preparation for labour/birth including pain management / birth plan, recognition of active labour, care of new baby, vitamin K prophylaxis, newborn screening tests, postnatal self-care, awareness of ‘baby blues’ and postnatal depression

At 38 weeks: options for management of prolonged pregnancy

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6
Q

Outline what is done at the booking appointment (8-10 weeks)

A

For detecting risk factors - high risk pathway or extra surveillance. May identify social difficulties & discuss parental wishes for pregnancy.

1) Past obstetric history 2) Medical & surgical history e.g. gynaecological procedures, blood transfusions - may have developed red cell antibodies) 3) FHx: thalassaemia, CF, sickle cell anaemia, chromosomal disorders etc.
4) Current pregnancy: LMP + menstrual history (EDD)
5) Social & drug history (support / cessation services)
6) Mental health: schizophrenia, bipolar, postnatal depression/psychosis, family history
7) Examination: pulse, BP, BMI (>30 has increased risk complications), abdominal examination (approximation of uterine size, rarely masses/abnormalities) 8) USS: fetal viability, gestational age and multiple pregnancy. May also measure nuchal translucency where appropriate & diagnosis of fetal anomalies e.g. anencephaly.
9) Urinalysis 10) Bloods 11) Discuss screening options for chromosomal & structural abnormalities 12) Supplementation: offer vitamin D 10mcg/day from booking, Folic acid for first 12 weeks. Iron only for specific indications (IDA). 13) Food hygiene 14) Lifestyle advice. 15) Discuss antenatal classes & breastfeeding workshops

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7
Q

What general lifestyle advice can be given at booking?

A

Balanced diet, no smoking/drinking/recreational drugs, foods with plenty of iron, calcium & folic acid (greens, brown rice, fortified cereals). Aim for 2x fish week (at least 1 oily), avoid high vitamin A (liver / vitamin supplements) & 300mg/day caffeine limit.

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8
Q

What dietary advice can be given at booking?

A

avoid raw seafood, unpasteurised juice/cider, undercooked meat & poultry. Be selective with smoked seafood, meat spreads or pate. Do NOT have unpasteurised milk or raw sprouts. Tailor homemade ice cream recipes. Reheat hot dogs & lunch meats. Food poisoning in pregnancy: campylobacter, E. coli, listeria, salmonella, toxoplasmosis (avoid cat faeces, wash hands / fruit / veg, gloves for handling soil)

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9
Q

What is checked on urinalysis at booking?

A

Protein & glucose

Early pregnancy: UTI, occasionally hyperglycaemia)

Culture if positive for asymptomatic bacteriuria.

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10
Q

What blood tests are done at booking?

A

FBC (anaemia, thrombocytopenia)
Blood group, Rhesus status & antibodies,
Rubella & immunity (if risk of having primary infection during pregnancy – offered vaccination at delivery), Syphilis (positive - GUM referral)
Gonorrhoea, chlamydia, HIV,
Hep B surface antigen (if positive, counselling of family & neonatal vaccination).

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11
Q

After booking, what appointments are needed?

A

10-13+6 weeks: early scan to confirm dates

11-13+6 weeks: Down’s screening including nuchal scan

16 weeks: Information on anomaly scan & blood results (consider iron if Hb <11g/dl). Routine care.

18-20+6 weeks: Anomaly scan

25 (primip): Routine care + SFH

28 weeks: Routine care + SFH. Second screen for anaemia & atypical red cell alloantibodies (consdier iron if Hb <10.5g/d;). First dose of anti-D prophylaxis if Rh -ve.

31 (primip): Routine care

34 weeks: Routine care, ?second dose of anti-D
Information on labour & birth plan

36 weeks: Routine care. Check presentation: offer ECV if indicated. Info on breast feeding, vitamin K, ‘baby-blues’

38 weeks: Routine care

40 (only if primip): Routine care as above, discussion about options for prolonged pregnancy

41: Routine care, discuss labour plans + possibility of induction

Routine care = BP, urine dip (+ SFH from 25 weeks)

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12
Q

What screening is done on neonates after birth?

A

Newborn examination: within 72 hours then at 6-8 weeks
Heelprick test: (CF, thyroid, metabolic)
Newborn hearing

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13
Q

Define screening

A

Identifying healthy people who may be at increased risk of disease, then offering information, further diagnostic tests and appropriate treatment to reduce their risk and/or complications arising from the condition

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14
Q

In the first trimester, what screening / procedures / imaging is done?

A

Weeks 10-12

Bloods - also consider: Hb electrophoresis (for sickle cell anaemia / thalassaemia, offered to all women or restricted to certain ethnic origins), PPD (tuberculosis), other STIs, thyroid screen, vitamin D, early glucose challenge, varicella antibody, genetic screening, CVS if required.

Dating USS if unknown LMP or size-dates discrepancy on initial exam

Weeks 11-13
1st trim USS + maternal serum screening

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15
Q

In the second trimester, what screening / procedures / imaging is done?

A

Weeks 16-18: Maternal serum alpha fetal protein

Weeks 15-22: Quadruple marker serum screening, amniocentesis for chromosomal abnormalities, if required

Weeks 18-20: Fetal anomaly USS

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16
Q

In the 3rd trimester, what screening / procedures / imaging is done?

A

28 weeks: FBC, antibody testing, glucose challenge test
Syphilis screen, HIV antibody testing (if high risk), administer anti-D if needed

33-36 weeks: Determine newborn care provider, offer childbirth education courses, gonorrhoea & chlamydia screen (if high risk),
36+ Determine fetal presentation
35-37 Group B streptococcus screen
41 Offer IOL

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17
Q

What are some common antenatal complaints?

A
o Backache
o Pelvic girdle pain (PGP)
o Carpal tunnel syndrome
o Constipation
o Haemorrhoids
o Heartburn
o Itching
o Leg cramps
o Nausea and vomiting
o Vaginal discharge
o Varicose veins
o Dermatoses (PEP, prurigo of pregnancy, pruritic folliculitis, pemphigoid gestationis)
18
Q

What are dermatoses of pregnancy?

A

Heterogenous group of pruritic inflammatory dermatoses that occur exclusively during pregnancy and/or immediate postpartum period.

Includes: pemphigoid gestationis, polymorphic eruption of pregnancy (PUPPP – pruritic urticarial papules and plaques of pregnancy), atopic eruption of pregnancy (eczema of pregnancy, prurigo of pregnancy, pruritic folliculitis of pregnancy), intrahepatic cholestasis of pregnancy, pustular psoriasis of pregnancy.

19
Q

What is pemphigoid gestationis?

cause, pathophysiology

A

Rare autoimmune bullous disease (2nd or 3rd trimester), may be associated with fetal risk & preterm birth. ~1 in 20,000/50,000 pregnancies, (and in minority of cases may occur as paraneoplastic manifestation in women with trophoblastic tumours). Binding of antibodies to antigens within the basement membrane > inflammatory cascade > separation of epidermis from dermis (as in bullous pemphigoid).

  • circulating IgG1 autoantibodies against BP180 or collagen XVII (180 kilodalton bullous pemphigoid antigen), a transmembrane hemidesmosomal glycoprotein expressed in basement membrane. Majority of patient sera bind extracellular NC16A epitope, but some bind other epitopes on BP180 (intracellular and extracellular).
  • Placenta likely the primary site of autoimmunity (antibodies also bind to basement membrane of chorionic and amniotic epithelia – both of ectodermal origin).?paternal MHC class II found on chorionic villi induce maternal antibodies to the amniotic basement membrane
  • antibodies then cross-react with skin > maternal (and sometimes newborn) disease. Disease is associated with a specific class II HLA phenotype.
20
Q

Symptoms, diagnosis and Tx of pemphigoid gestationis?

A
  • Most often in the 2nd or 3rd trimester
  • Intense pruritis may precede onset of visible lesions
  • Rash typically begins on trunk as urticarial plaques or papules surrounding umbilicus (early phase can sometimes mimic PEP)
  • Vesicles may also be present
  • Lesions may be seen on palms & soles but rarely on face or mucous membranes (entire body surface may be involved but mucous membranes usually spared)
  • Eruption spreads rapidly + forms tense blisters (some patients may not have blisters but have large plaques)

May remit before delivery, however, 75% flare postpartum & at least 25% flare with oral contraceptive pills or during menses. Most resolve spontaneously in weeks-months following delivery and usually recurs with subsequent pregnancies (often worse) but may also skip pregnancies.

Dx: combination of clinical findings, histopathology and direct immunofluorescence (DIF) of perilesional skin biopsy, and serum levels of anti-BP180 antibodies by enzyme-linked immunosorbent assay (BP180 NC16A ELISA).

Treatment: High potency topical corticosteroids – systemic if topicals not effective

Prognosis generally good for fetus despite increased risk of prematurity and small for gestational age babies due to mild placental failure. There is no increased risk of miscarriage.

21
Q

What is Polymorphic eruption of Pregnancy (PEP)?

A

Also called pruritic urticarial papules and plaques of pregnancy (PUPPP): benign, self-limiting pruritic inflammatory disorder that usually affects primips in last few weeks (mean onset 35 weeks) or immediately post-partum (also rare case reports of 1st and 2nd trimester disease).

Relatively common (1 in 160-300 pregnancies) & ¾ with classic type are nulliparous. More common with excessive stretching, especially in women with multiple gestation. Other than maternal pruritis, there is no increased risk of maternal or fetal morbidity & recurrence is rare.

  • Extremely pruritic, erythematous papules within striae
  • Abdominal striae are the most common initial site (with periumbilical sparing) and may be the only initial site
  • The lesions then spread to the extremities, chest and back and coalesce to form urticarial plaques.
  • Face, palms + soles are usually spared
  • White halos often surround the erythematous papules in patients with fair skin
  • Over the course of the disease, approximately ½ of pts develop more polymorphic lesions, including target-like lesions exhibiting 3 distinct rings / colour changes instead of a halo, or erythematous patches and vesicles

Eruption generally lasts 4-6 weeks and resolves within 2 weeks postpartum (but may last longer or resolve prior to delivery). Diagnosis usually clinical (history and exam) and skin biopsy generally not necessary (possible if diagnostic uncertainty) – no laboratory markers.

22
Q

Tx of PEP?

A

mid-to-high potency topical corticosteroids od. or bds. or in severe cases short course of systemic corticosteroids e.g. prednisone or prednisolone 0.5mg/kg/day for 1 week and tapered over 1-2 weeks. Chloramphenamine or loratadine and cetirizine may help control pruritis.

23
Q

What is atopic eruption of pregnancy (AEP)?

A

Unifying term that includes eczema in pregnancy, prurigo of pregnancy & pruritic folliculitis of pregnancy (previously considered distinct entities). None are associated with adverse effects on fetus. Eczematous or papular eruption in patients with an atopic background (remains controversial: personal or family history of seasonal rhinitis, asthma and/or atopic dermatitis). Starts early pregnancy, with 75% of cases occurring before the 3rd trimester. It tends to recur in subsequent pregnancies. It is the most common of the pregnancy dermatoses (50% of all cases).

  • 20% of cases = AEP is an exacerbation of a pre-existing atopic dermatitis
  • Not associated with adverse effects on fetus
  • May recur in subsequent pregnancies.

Presentations
o Eczema: eczematous eruption (E-type AEP) involving face, neck & flexural areas (similar to classic atopic dermatitis) - any of the skin may be affected & lesions may be eczematous patches or intact or excoriated papules (papules can be follicle based, grouped or scattered). Skin dryness always present (may be severe).
o Prurigo of pregnancy: less common presentation (P-type AEP): erythematous, excoriated nodules or papules on extensor surfaces of limbs & trunk. Lesions are grouped and may be crusted or appear eczematous. Usually resolves in immediate postpartum periods but can persist for up to 3 months.
o Pruritic folliculitis of pregnancy: rare presentation of AEP - follicular papulopustular eruption with scattered follicle-based papules & pustules similar to steroid induced acne (only midly pruritic). Eruption typically clears within two weeks of delivery. Lab testing generally not indicated but up to 70% may have elevated serum IgE, and if presenting with folliculitis, pustule should be cultured to exclude bacterial or candidal folliculitis.

Treatment: emollients, low-to-mid potency topical corticosteroids or oral antihistamines (chlorpheniramine or second-generation: loratadine and certirizine).

24
Q

What is intrahepatic cholestasis of pregnancy?

A

Obstetric cholestasis: only pregnancy dermatoses without primary skin changes. Severe, generalised pruritis, predominantly on palms & soles, and may present with excoriations secondary to scratching. ICP carries significant morbidity for fetus (prematurity, meconium-stained amniotic fluid, intrauterine demise, respiratory distress syndrome). Maternal prognosis generally favourable (one study suggests increased risk of later hepatobiliary disease).

25
Q

Role of folic acid in pregnancy?

A

Green, leafy vegetables are a good source. Converted to tetrahydrofolate (THF), which plays a key role in transfer of 1-carbon units (e.g. methyl, methylene and formyl groups) to the essential substrates involved in the synthesis of DNA & RNA. Important for prevention of neural tube defects: advised that all women take standard dose of 0.4mg (400mcg) folic acid a day pre-conception and continue until 12/13 weeks. Folic acid is started pre-conception because the neural tube is formed within the first 28 days of an embryo’s development – and thus any defect may already be present if a woman waits until her missed period.

Certain women are at an increased risk of neural tube defects and thus should take an increased dose of 5mg folic acid (until week 12). Women falling into this category include:

  • Previous child with neural tube defect
  • Either partner has a NTD / FHx
  • Diabetes mellitus
  • Woman on antiepileptic
  • Obese (BMI >30)
  • HIV positive taking co-trimoxazole
  • Sickle cell
  • Thalassaemia trait
  • Coeliac disease

Causes of folic acid deficiency: phenytoin, methotrexate, pregnancy & alcohol excess

Consequences of deficiency: macrocytic megaloblastic anaemia, neural tube defects

26
Q

What is Pustular Psoriasis of Pregnancy (PPP)?

A

Formerly known as impetigo herpetiformis, extremely rare variant of generalised pustular psoriasis occurring during pregnancy – typically presents 3rd trimester but may occur earlier or in the immediate postpartum period.

Symmetric erythematous plaques studded at periphery with sterile pustules in a circinate pattern. Plaques then enlarge from periphery as centre becomes eroded and crusted. There may be concentric rings of pustules (typically sterile). Eruption begins in flexural areas and spreads centrifugally – trunk & extremities usually involved while hands, feet & face usually spared. Oral and oesophageal erosions may occur – nails may become oncyolytic (lifting of the nail plate from the nail bed) and pitting also described. Pruritis usually absent but systemic symptoms are severe: malaise, fever, anorexia, nausea, vomiting, diarrhoea + tetany.
- Leukocytosis and elevated ESR are common. Hypocalcaemia may be present, possibly related to hypoparothyroidism, and can lead to tetany, delirium & seizures. Albuminuria, hypoalbuminaemia, pyuria and haematuria occasionally occur.

o Usually remits postpartum but may flare after delivery
o Placental insufficiency with severe sequlae e.g. miscarriage, fetal growth restriction or stillbirth may occur

27
Q

Dx and Tx of Pustular Psoriasis of Pregnancy (PPP)?

A

Diagnosis can be made clinically but biopsy also suggested due to consequences of disease & treatment to maternal / fetal health.

Tx: prompt as associated risk for fetus (fetal monitoring, USS and biophysical profiles needed), hypocalcaemia corrected if present, maintain electrolyte balance. Early delivery sometimes required for symptoms + fetal safety. Corticosteroids or low dose cyclosporine recommended.

28
Q

What is polyhydramnios?

How does it present?

A
Polyhydramnios
Excessive amniotic fluid volume (1-2% of pregnancies)
o	Amniotic fluid index >20-25
o	Largest pocket fluid depth >8 or 10cm
o	Overall volume >1500-2000cm³
o	2 diameter pockets >50cm³

Some women experience: breathlessness, swollen feet, heartburn, constipation

Presentation: SFH large for dates, foetal parts difficult to palpate, rapid presentation in twin pregnancy suggests TTTs.

29
Q

Complications and causes of polyhydramnios?

A

Complications
o Cord prolapse
o Preterm labour (overexpanded uterus more excitable)
o Placental abruption (particularly after rupture of membranes where there is rapid decompression of the uterus: when performing amniotomy, ensure slow release of amniotic fluid)
o PPH: overstretched uterus does not contract sufficiently

Causes
o	Idiopathic (60-65%)
o	Foetal
o	Oesophageal atresia
o	Chromosomal abnormalities e.g. Down’s syndrome
o	Neural tube defects
o	TTTS in multiple pregnancy
o	Hydrops fetalis
o	Rhesus disease
o	Maternal
o	Diabetes (20-25%): pre-existing or gestational
o	Placental factors

Delivery in hospital is generally advised.

30
Q

Investigations for polyhydramnios?

A

USS for AFI and foetal wellbeing, other tests may be required for Dx e.g. blood glucose, Coomb’s test / Rhesus D if suspicion of haemolytic disease / foetal hydrops, infection screen (CMV, syphillis, rubella, toxoplasmosis, parvovirus B19), chromosomal abnormalities (genotyping)

31
Q

What is oligohydramnios?

How does it present?

A

Deficient amniotic fluid volume (1-5% of pregnancies at term, higher if >41 weeks)

o Amniotic fluid index <5

Tends to be asymptomatic other than decreased fetal movement, uterine size may also be less than expected for dates. Amnion nodosum (nodules on fetal surface of the amnion) also often present.

32
Q

Complications, causes and Tx of oligohydramnios?

A

Complications
o Fetal death
o Intrauterine growth restriction
o Cord compression
o Facial distortion (e.g. Potter syndrome)
o Limb contractures (if begins in early pregnancy)
o Delayed lung maturation (if begins early in pregnancy)
o Inability of fetus to tolerate labour > C-section

Causes
o Uteroplacental insufficiency (pre-eclampsia, chronic hypertension, abruption, thrombotic disorder) – growth restricted fetus may divert blood away from kidneys
o Drugs (e.g. NSAIDs, ACEIs)
o Postterm pregnancy
o Fetal malformations (particularly those reducing urine production)
o Fetal death
o Chromosomal abnormalities (e.g. aneuploidy)
o Premature rupture of the membranes
o Idiopathic

33
Q

Management of oligohydramnios?

A

‘simple maternal hydration appears to increase amniotic fluid volume and may be beneficial in management/prevention of oligohydramnios’.

Serial USS atleast every 4 weeks (every 2 weeks if growth restricted) to monitor growth. Weekly AFI measurements. Fetal monitoring with nonstress testing / biophysical profile weekly, delivery at term?

34
Q

What is breech presentation? how common?

A

Presenting for delivery with buttocks or feet first

Incidence decreases with gestation: 40% at 20 weeks, 25% at 28 weeks, but only 3-4% at term).

May be extended/frank breech (most common), flexed breech or footling breech (rarest but riskiest: 5-20% cord prolapse).

35
Q

Risk factors for breech?

A

Risk factors: prematurity, small for gestation age fetus, nulliparity, fetal congenital anomalies, multiple pregnancy, uterine malformations, fibroids, placenta praevia, poly/oligohydramnios

36
Q

Risks associated with breech - mother and baby?

A

Associated with increased morbidity + mortality for the mother
o Emergency C-section
o Placenta praevia

Associated with increased morbidity &amp; mortality for the baby
o Preterm birth
o Small fetal size
o Congenital anomalies
o Perinatal mortality
37
Q

Treatment of breech presentation? before birth

A

Treatment algorithm: diagnosed at term (36w) if <36 weeks many turn spontaneously

  1. Offer external cephalic version (ECV)
  2. Declined / unsuccessful ECV: offer information about mode of delivery
3. Assess for risk factors for poorer outcome in planned vaginal breech birth
o	Hyperextended neck on USS
o	High estimated fetal weight (>3.8kg)
o	Low estimated weight (<10th centile)
o	Footling presentation 
o	Evidence of antenatal fetal compromise

Presence of skilled birth attendant essential for safe vaginal breech birth; units with limited access to experienced staff should inform of greater risk and offer antenatal referral to unit with greater experience

38
Q

ECV info?

A

50% success rate

Cross-matching & USS before procedure, intermittent CTG monitoring.

Risks: severe maternal discomfort, abruption, preterm labour, PROM, cord entanglement

Contraindications: placenta praevia, recent APH, abnormal fetal monitoring, ruptured membranes, multiple pregnancy, pre-eclampsia, oligohydramnios

39
Q

Information about mode of delivery if breech baby?

A

Planned C-section leads to small reduction in perinatal mortality due to 3 factors (balance against potential adverse consequences)
o Avoidance of stillbirth >39weeks
o Avoidance of intrapartum risks
o Avoidance of risks of vaginal breech birth (this is the only factor unique to breech presentations)

(Perinatal mortality is 0.05% with C-section after 39 weeks, ~0.2% with planned vaginal breech birth (0.1% planned vaginal cephalic birth).

Planned vaginal breech birth increases risk of low Apgar scores + serious short-term complications, but has not been shown to increase the risk of long-term morbidity.

Planned C-section for breech at term has small increase in immediate complications for mother compared with planned vaginal birth (however, risk is highest with emergency C-section which is needed in ~40% of women with vaginal breech birth)

C-section increases risk of complications in future pregnancy, including risks of opting for VBAC, increased complications at repeat C-section and risk of an abnormally invasive placenta

C-section been associated with small increase in risk of stillbirth for subsequent babies, but this may not be casual

40
Q

Treatment of unplanned vaginal breech labour? (~25% not diagnosed until labour)

A
  1. Women near or in active 2nd stage of labour: do not routinely offer C-section
  2. If time / circumstance permits: position of neck, legs and weight should be estimated on USS and woman counselled as with planned vaginal breech
  3. Induction not usually recommended but augmentation of slow progress with oxytocin should only be considered if low contraction frequency in presence of epidural
  4. Effect of epidural unclear but likely to increase risk of intervention
  5. Recommend birth in hospital with facilities for immediate C-section but birth in operating theatre not routinely recommended
  6. Adequate descent of the breech in the passive second stage is a prerequisite for encouragement of the active second stage (first stage should be managed according to same principles as with cephalic presentation, but amniotomy reserved for definite clinical indications; consider C-section where progress is slow. If breech not visible within 2 hours of the passive second stage, C-section recommended).
  7. Assistance without traction required if delay or evidence of poor fetal condition (obstetricians and midwives should be familiar with the techniques that can assist vaginal breech birth)
  8. Routine C-section for breech presentation in spontaneous preterm labour is NOT recommended (but may be recommended for planned pre-term C-section where planned due to maternal/fetal compromise). Singleton preterm breech labour should be managed as with a term breech.
  9. Planned C-section where presenting twin is breech is recommended, but not for a breech first twin in spontaneous labour
  10. Routine C-section for breech second twin is not recommended for term or preterm deliveries.