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Oxford handbook O&G > Chapter 2 - Complications in pregnancy > Flashcards

Chapter 2 - Complications in pregnancy Flashcards

1
Q

What recommendations can you give for N/V of pregnancy?

A
  • That it tends to resolve by 16-20w
  • It not associated with poor outcomes
  • Some women need to be admitted if it is severe (hyperemesis
    gravidarum)
  • Eat small meals
  • Increase fluid intake
  • Try ginger
  • Acupressure
  • Anti-emetics (prochlorperazine, promethazine, metoclopramide).
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2
Q

What causes N/V in pregnancy?

A
  • It is believed to be caused by hCG

- It is worse in multiple or molar pregnancies (where hCG is higher)

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3
Q

Advice for GERD in pregnancy

A

Lifestyle modifi cation (e.g. sleep propped up, avoid spicy food)

Alginate preparations and simple antacids

If severe, H2 receptor antagonists (ranitidine).

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4
Q

Advice for constipation in pregnancy

A
  • Usually improves with gestation
  • Caused by progesterone reducing smooth muscle tone and bowel movements
  • Made worse by iron supplements
  • Increase fruit, fibre and water intake
  • Fiber supplements
  • Osmotic laxatives (lactulose)
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5
Q

Advice for backache and sciatica

A
  • lifestyle modifi cation (e.g. sleeping positions)
  • alternative therapies including relaxation and massage
  • physiotherapy input (e.g. back care classes)
  • simple analgesia.
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6
Q

What causes carpal tunnel syndrome in pregnancy?

A
  • Due to oedema compressing the median nerve

- Wrist splints may help

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7
Q

Suggest advice for haemorrhoids in pregnancy

A
  • Avoid constipation early in pregnancy
  • ice packs and digital reduction
  • suppositories and topical relief
  • if thrombosed, refer for surgery
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8
Q

Explain the cause of varicose veins in pregnancy and management

A
  • Progesterone relaxes vasculature and the fetal mass effect decreasing venous return
  • Regular exercise
  • Compression hosiery
  • thromboprophylaxis if other risk factors present
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9
Q

Why are urinary symptoms more common in the first T?

A
  • increased glomerular filtration rate and uterus pressing on the bladder
  • stress incontinence may occur in the 3rd T due to pressure on the pelvic floor
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10
Q

Management of vaginal discharge

A
  • increases due to increased blood flow to vagina and cervix
  • Should be white/clear
  • Exclude rupture of membranes
  • Exclude STI and candidiasis
  • Reassure
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11
Q

Management for a new rash in pregnancy

A
  • full hx and examination to exclude infectious causes and obstetric cholestasis
  • emolients and simple anti-itch cream
  • reassure - very common and usually resolves after delivery
  • referral if severe
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12
Q

Define antepartum haemorrhage

A

Bleeding from the genital tract in pregnancy at >24 weeks before labour

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13
Q

5 Causes of antepartum haemorrhage

A

1) unexplained (97%) - possibly minor placental abruptions most bleeding in concealed
2) placenta praevia (1%) may be rapid and severe
3) placental abruption (1%)
4) vasa praevia
5) incidental ectropion

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14
Q

What causes vasa praevia?

A

Occurs when fetal vessels run in membranes below the presenting fetal part

  • May present with PV after rupture of fetal membranes and fetal distress
  • Mortality 33-100%
  • RF: low lying placenta, multiple pregnancy, IVF and bilobed placentas
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15
Q

Antepartum haemorrhage assessment?

A

History

  • Gestation
  • Amount of bleeding
  • Initiating factors
  • Pain
  • Fetal movements
  • Date of last smear
  • Previous PV bleeds
  • Previous uterine surgery
  • Smoking/cocaine
  • Blood group/resus status
  • Previous obs hx
  • Position of placenta if known

Examination

  • BP, pulse, haemodynamic compromise, uterine palpation (size, tenderness, fetal lie, presenting part)
  • **DON’T PERFORM PV UNTIL EXCLUDED PP (placenta praevia)
  • Speculum examination after PP excluded - assess for trauma, polyps, ectropian
  • Fetal heart beat (if heard = >26wks)
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16
Q

Define placenta praevia

A

When the placenta is inserted wholly or in part into the lower segment of the uterus

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17
Q

What are the grades of placenta praevia?

A

Major

  • Placenta is over the cervical os
  • Cervical dilation would cases a catastrophic bleed

Minor
- Placenta lies in the lower segment close to the os

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18
Q

How do you diagnose PP?

A

Transvaginal USS is safe and is more accurate than transabdominal

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19
Q

Do women with PP have to be admitted?

A

Women with major PP who have previously bled should be admitted from 34wks

Asymptomatic major PP women could stay at home if:

  • they live close
  • if they are aware of the risks
  • have constant companion
  • have a telephone and transport
  • CS is usually needed if the placenta is <2cm from the internal os
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20
Q

Describe the management of a minor AH

A

If minor and settling and no signs of compromise

1) US for fetal growth/vol amniotic fluid + placenta position
2) Umbilical artery doppler (function of placenta)
3) FBC + Kleihauer testing if RhD -ve to determine extent of haemorrhage and if more anti-D is needed
3) Group and save
4) coag screen (if abruption suspected)

**ALL RhD -ve women reuire 500IU anti-D immunoglobulin unless sensitized. More anti-D may be needed depending on Kleihauer

5) Admit for 24hrs (risk of re-bleed highest)
6) Discharge once stable and bleeding stopped. With increased fetal surveillance

** women with previous APH are at high risk

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21
Q

Describe the Kleihauer Test

A

Is a blood test from EDTA bottles that can determine the extent of feto-maternal haemorrhage (break in the placenta barrier where fetal blood has entered the maternal blood risking sensitisation of RhD -ve women)

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22
Q

True or False:

Women with APH are at increased risk of PPH

A

TRUE : they will require additional monitoring

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23
Q

Define placental abruption

A

Placenta separates partly or completely from uterus before delivery. Blood then accumulates behind the placenta in the uterine cavitity or is lost through the cervix

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24
Q

Give the types of placental abruption

A

1) Concealed (no external bleeding) <20%

2) Revealed (vaginal bleeding)

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25
Q

What are the presenting features of placental abruption?

A

Sudden/Constant/Severe Abdominal Pain

  • Posterior placenta –> backache
  • tender uterus
  • uterine activity
  • hard uterus (woody)
  • 50% occur in labour
  • Bleeding is variable
  • maternal shock
  • fetal distress (proceeds death)
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26
Q

Management of abruption

A
  • Admit all women with vaginal bleeding or unexplained abdo pain
  • Fetal CTG
  • USS asap
  • Access + bloods
  • If fetal distress or maternal compromise –> resus + deliver
  • If no compromise consider delivery by term
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27
Q

Describe the changes in BP during pregnancy and after delivery

A

Drops initially due to reduction in vascular resistance

After 24weeks stroke vol increases and BP rises

After delivery BP drops but may peak again 3-4 days post-partum

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28
Q

Describe the correct position to measure BP

A

Upright

OR

Supine with left sided tilt to avoid IVC compression reducing venous return.

  • Arm must be at the level of the heart
  • Correct sizing

Beware of high BP in booking - check not chronically hypertensive

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29
Q

Define preganancy induced hypertension

A

Hypertension >/= 140/90 in the second half of pregnancy in the absence of proteinuria or markers of pre-eclampsia

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30
Q

TRUE or FALSE:

PIH increases risk of pre-eclampsia

A

TRUE

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31
Q

TRUE or FALSE:

Patients who develop PIH later in pregnancy are at increased risk of developing pre-eclampsia than earlier

A

FALSE

The risk of developing pre-eclampsia is higher with an earlier onset of hypertension

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32
Q

When should delivery be aimed for in women with PIH?

A

EDD

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33
Q

“will my high blood pressure continue to be high after pregnancy? will i need to be on long term meds?”

A

Most womens BP returns to normal within 6 weeks of delivery and treatment is not needed unless undiagnosed high BP before pregnancy.

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34
Q

TRUE or FALSE:

PIH increases risk of pre-eclampsia but chronic hypertension dose not.

A

FALSE: both increase risk of pre-eclampsia

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35
Q

Why is PIH more common now?

A

Aging population - chronic hypertension

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36
Q

What factors need to be considered in post-partum hypertension?

A

Is it physiological, pre-excisting chronic HT, D3-5 common rise or new onset pre-eclampsia

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37
Q

Is methyldopa safe to continue postnatally?

A

It should be changed to BB due to risk of post-natal depression

  • Captopril and Nifedipine are safe to use with breast feeding
  • arrange follow up 6weeks (by which case most have resolved)
  • if still high investigate secondary causes
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38
Q

Name the 5 safe commonly used anti-hypertensives used in pregnancy

A

1) Labetalol
2) Methyldopa
3) Nifedipine
4) Hydralazine
5) Atenolol

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39
Q

Are ACE inhibitors safe in pregnancy?

A

NO, only post partum is captopril safe

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40
Q

When should atenolol and labetalol be avoided?

A

In patients with asthma

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41
Q

What is the prescription range for labetalol?

A

100mg BD –> 600mg QDS

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42
Q

How can you manage severe refractory hypertension?

A

IV labetalol

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43
Q

What is the prescription range for methyldopa?

A

250mg bd up to 1g tds

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44
Q

What is the prescription range for nifedipine?

A

10mg BD up to 30mg tds

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45
Q

What is the prescription range for atenolol?

A

50-100mg od

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46
Q

What are the common side-effects of nifedipine?

A

Tachycardia, flushing,

headache

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47
Q

What are the common side-effects of hydralazine?

A

Tachycardia, pounding
heartbeat, headache,
diarrhoea

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48
Q

Which anti-hypertensives are safe for breast-feeding?

A

labetolol, methyldopa, nifedipine, hydralazine, atenolol and captopril

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49
Q

When should you treat hypertension?

A

> /= 160/110

Escalate treatment until BP under this. DO NOT AIM below 120/80

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50
Q

TRUE OR FALSE:

Treatment of BP protects women from pre-eclampsia and its complications

A

FALSE

- Treatment of BP protects women from the adverse effects of high BP, it does not alter the course of pre-eclampsia

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51
Q

Define pre-eclampsia

A

BP >140/90 and >300mg protienuria in 24hrs

  • *If already hypertensive
  • BP increase of >30/15**
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52
Q

What is the incidence of pre-eclampsia?

A

5% of pregnancies

- severe = 1% of pregnancies

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53
Q

What are the increased chances of women with pre-eclamsia in a previous pregnancies suffering in subsequent?

A

7x increased risk

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54
Q

Which bloods should be included in pre-eclampsia screening?

A
  • LOW Plasma protein-A (PAPP-A)
  • HIGH uric acid
  • LOW platelets
  • HIGH Hb

interest in VEGF, placental growth factor and soluble FM-like tyrosine kinase

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55
Q

How may you differentiate PIH from pre-eclampsia prior to the development of proteinura?

A

high uric acid, low platelets and high Hb suggest pre-eclampsia over PIH

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56
Q

What is the most predictive test for pre-eclampsia?

A

RFs + PAPP-A + uterine arteries at 12weeks

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57
Q

Is any treatment recommended to prevent pre-eclampsia?

A

Women who have had severe early-onset pre-eclampsia should be offered low dose aspirin (75mg PO OD) before 16 weeks

58
Q

Describe the trial studying the effect of Aspirin in reducing Pre-eclampsia

A

The ASPRE Trial in 2017 randomised approx 1700 women to Aspirin 150mg OD from Wks16-36 vs placebo and found a significant reduction in the development in Pre-eclampsia by week 37

  • No significant difference in adverse effects between groups but it was not highly powered
59
Q

Give 3 secondary causes of hypertension

A

1) Renal disease
2) Cardiac disease (coarctation)
3) Endocrine (cushings, conns)

60
Q

Give 3 complications in pregnancy caused by chronic hypertension

A

1) superimposed pre-eclampsoa
2) Fetal growth restriction
3) Placental abruption

61
Q

Give 10 RF of pre-eclampsia

A

1) Previous severe/early onset pre-eclampsia (7x)
2) >40 or teenager
3) FH (mother or sister) (4x)
4) BMI >30 (2x)
5) Primiparity (2x)
6) Multiple pregnancy (5x)
7) Fetal hydrops
8) Hydatidiform mole
9) Ht
10) Renal disease
11) DM
12) anti-phospholipid
13) thrombophilias
14) connective tissue disease

62
Q

Symptoms of pre-eclampsia

A

Most are asymptomatic, symptoms usually occur if severe.

  • Headache
  • Visual disturbance
  • Epigastric or RUQ pain
  • N/V
  • Rapid oedema (face)
63
Q

Signs of pre-eclampsia

A
  • Hypertension >140/90 (>160/110 severe)
  • Proteinuria >300mg in 24hrs
  • Facial oedema
  • Epigastric/RUQ tenderness = liver involvement and capsule distension
  • Confusion
  • Hyperreflexia +/- clonus (>3 beats) = cerebral irritability
  • Uterine tenderness or vaginal bleeding from placental abruption
  • Fetal growth restriction on US, if <36wks
64
Q

What investigations should you order for a patient you are working up for pre-eclampsia

A

FBC - high hb (haemoconcentration), low platelets, anaemia if haemolysis (HELLP)

Coagulation profile - Prolonged PT and APTT

Biochem - high urate, urea/creatinine, transaminitis, high LDH (haemolysis)

Urine - proteinuria

65
Q

Name 5 severe complications of pre-eclampsia

A

1) Eclampsia
2) HELLP
3) Cerebral haemorrhage
4) IUGR and fetal compromise
5) Renal failure
6) Placental abruption

66
Q

when would outpatient management of pre-eclampsia be appropriate?

A

If:

1) BP <160/110 + controllable
2) No or low proteinuria
3) Asymptomatic

67
Q

Describe outpatient management of pre-eclampsia

A
  • Warn about symptoms to look for

- Weekly BP, urine and bloods

68
Q

When is it advised for women with mild pre-eclampsia to be admitted?

A

Once significant proteinuria occurs

  • > 2+ protein
  • > 300mg
69
Q

How do you manage mild-mod pre-eclampsia?

A
  • Inpatient management
  • 4-hrly BP
  • 24hr urine collection
  • Daily urinalysis
  • Daily fetal assessments + CTG
  • Bloods every 2-3days unless symptoms worsen
  • Twice a week doppler/liquor volume
  • 2-weekly growth US
70
Q

When should anti-hypertensives be started?

A

If BP increases to >160 systolic OR 110 diastolic

doesn’t cure, just prevents complications

71
Q

What is the definition of severe pre-eclampsia?

A

BP >160 or >110 diastolic in the presence of significant proteinuria (>1g/24hrs or > 2+ on dipstick) or if complications occur

**must involve a senior **

72
Q

What is the treatment of pre-eclampsia?

A

Delivery (may worsen in the 24hrs after delivery) is the only treatment

73
Q

What are the indications for immediate delivery in pre-eclampsia?

A
  • Worsening thrombocytopaenia or coagulopathy.
  • Worsening liver or renal function.
  • Severe maternal symptoms, especially epigastric pain with abnormal LFTs.
  • HELLP syndrome or eclampsia.
  • Fetal reasons such as abnormal CTG or reversed umbilical artery
    end diastolic flow.
74
Q

How would you treat severe pre-eclampsia?

A

1) need a senior
2) FBC, U&E, LFTs, clotting
3) Strict fluid balance
4) CTG monitoring
5) Control BP
- PO nifedipine 10mg (give 2-3x 30mins apart)
- IV labetolol infusion (methyldopa if asthmatic)
6) US fetus (IUGR, fetal and umbilical artery doppler)

**if <34weeks give steroids and manage expectantly

75
Q

Define eclampsia

A

The occurrence of a tonic-clonic seizure in association with pre-eclampsia.

It is s severe disease causing death due to blood loss, intracranial haemorrhage or HELLP

make sure you know the hospital protocol and where the eclampsia box is

76
Q

Define HELLP syndrome

A

A serious complication regarded by most as a variant of severe
pre-eclampsia which manifests with haemolysis (H), elevated liver
enzymes (EL), and low platelets (LP).

77
Q

Incidence of HELLP in pre-eclamptics

A

5-20%

78
Q

Describe the presentation of HELLP

A
  • Liver enzymes increase and platelets decrease before haemolysis occurs.
  • Syndrome usually self-limiting, but permanent liver or renal damage
    may occur.
  • Symptoms include:
    • epigastric or RUQ pain (65%)
    • nausea and vomiting (35%)
    • urine is ‘tea-coloured’ due to haemolysis.
  • Signs include:
    • tenderness in RUQ
    • increased BP and other features of pre-eclampsia.
    • Eclampsia may co-exist.
  • Delivery is indicated.
  • Treatment is supportive and as for eclampsia (magnesium sulfate
    (MgSO 4 ) is indicated).
  • Platelet may be very low, but platelet infusions are only required if bleeding, or for surgery and <40.
79
Q

How do you manage eclampsia?

A

1) call for help
2) ABC approach + vascular access
3) FBC, LFTs, U&E, clotting
3) MgSO4 (control and prevent further fits)
- 4g loading over 5-10mins
- 1g/h infusion for 24hrs
- if further fits occur give 2g bolus
- therapeutic range 2-4mmol/L)
4) Diazepam for repeated seizures
5) BP, pulse, RR, O2 sat monitoring
6) Urine dip
7) Reflexes for Mg toxicity (confusion, loss of reflexes, resp depression and low BP)
- Half/stop infusion if oliguric (<20mL/h) or raised creatinine
- Tx 1g calcium gluconate over 10mins
8) Treat hypertension (PO nifedipine, IV labetalol)
9) fluid restrict (<1ml/kg/hr) - due to pulmonary oedema risk
10) CVC?
11) deliver once stable
12) if in HELLP, consider high dose steroids

**third stage should be given oxytocin not syntometrine or ergometrine (increases BP)

80
Q

Incidence of multiple pregnancy

A

1 in 34 babies

81
Q

What are the predisposing factors of multiple pregnancy?

A
  • Hx
  • FHx
  • Increasing parity
  • Increasing age
  • Japanese or nigerian
  • Clomiphene, IUI, IVF
82
Q

The type of twins resulting from 2 ovas being fertilised by different sperm

A

Dizygotic twins

–> separate amioniotic membranes and placentas (dichorionic and diamniotic—DCDA)

83
Q

The type of twins resulting from the division of one embryo into two

A

Monozygotic twins

84
Q

Do all monozygotic twins share placentas and AM

A

Whether they share the same amniotic membrane and/or chorion depends on the stage of development when the embryo divides.

  • < 3 days l DCDA 30%.
  • 4 –7 days l monochorionic, diamniotic (MCDA) 70%.
  • 8 –12 days l monochorionic, monoamniotic (MCMA) <1%.
  • > 12 days l conjoined twins (very rare).
85
Q

Signs and symptoms of multiple pregnancy

A
  • Hyperemesis gravidarum.
  • Uterus is larger than expected for dates.
  • Three or more fetal poles may be palpable at >24wks.
  • Two fetal hearts may be heard on auscultation.
86
Q

How do you determine chorionicity?

A

On US:
• Obviously widely separated sacs or placentae—DC.
• Membrane insertion showing the lambda (λ) sign—DC.
• Absence of λ sign <14wks diagnostic of MC.
• Fetuses of different sex—DC (dizygotic).

87
Q

Advice for mutli pregnant

A
  • consider regular iron and folate
  • Aspirin if indicated
  • Increased no of growth checks
  • offer delivery at 37-38weeks
88
Q

What are the maternal risks associated with multiple pregnancy?

A
  • Hyperemesis gravidarum.
  • Anaemia.
  • Pre-eclampsia (5× greater risk with twins than singletons).
  • Gestational diabetes.
  • Polyhydramnios.
  • Placenta praevia.
  • Antepartum and post-partum haemorrhage.
  • Operative delivery.
89
Q

What are the fetal risks associated with multiple pregnancy?

A

All fetal risks increased with MC twins.

• Increased Risk of miscarriage : especially with MC twins.
• Congenital abnormalities more common only in MC twins including:
• neural tube defects
• cardiac abnormalities
• gastrointestinal atresia.
• Increased IUGR: up to 25% of twins.
• Preterm labour: main cause of perinatal morbidity and mortality:
• Increased Perinatal mortality:
• Increased risk of intrauterine death (stillbirth):
• Increased risk of disability (mainly, but not entirely, due to prematurity and
low birth weight).
• Increased Incidence of cerebral palsy (CP):
• Vanishing twin syndrome: one twin apparently being reabsorbed at an
early gestation (1st trimester).

90
Q

Complications of monochorionic twins

A

1) Twin to twin transfusion
2) Selective IUGR
3) Termination
4) Twin reversed arterial perfusion (TRAP)

91
Q

Effects of twin-to-twin transfusion on the fetus

A

Donor twin
• Hypovolaemic and anaemic.
• Oligohydramnios: appear ‘stuck’ to the placenta or uterine wall.
• Growth restriction.

Recipient twin
• Hypervolaemic and polycythaemic.
• Large bladder and polyhydramnios.
• Cardiac overload and failure.
• Evidence of fetal hydrops (ascites, pleural, and pericardial effusions).
• This twin is often more at risk than the donor.

92
Q

Describe the effects of intrauterine death of a twin

A

• Dichorionic: the death of one twin in the 1st trimester or early part
of the 2nd does not appear to adversely affect the remaining fetus.
Loss in the late part of the 2nd or 3rd trimester usually precipitates
labour, with 90% having delivered within 3wks.
• M onochorionic: because of the shared circulation, subsequent death
or neurological damage from hypovolaemia follows in up to 25%,
where one of the pair dies. Delivery does not decrease the risk of
brain injury.

93
Q

Describe the intrapartum risks associated with multiple pregnancy

A
  • Malpresentation.
  • Fetal hypoxia in second twin after delivery of the first.
  • Cord prolapse.
  • Operative delivery.
  • Post-partum haemorrhage.
  • Rare:
  • cord entanglement (MCMA twins only)
  • head entrapment with each other: ‘locked twins’
  • fetal exsanguination due to vasa praevia.
94
Q

Describe the management of labour and delivery for twins

A
  • Induce at 38weeks (most
    delivered spontaneously before then)
  • IV access and Group and Save.
  • CTG monitoring
  • fetal scalp monitoring may help
  • Determine the lie of the second after the first is out
  • The second must be delivered after the first to ensure hypoxia does not ensue
  • forceps or ventouse if fetal distress occurs in the second twin
  • increased risk of uterine atony, syntometrine and
    prophylactic oxytocin infusion is recommended.
95
Q

Describe the types of breech

A

1) extended breech - (70%) forward bend, bum presenting
2) flexed breech - childs pose, bum and feet presenting
3) footling breech - one leg flexed one extended

96
Q

Causes of breech presentation

A
  • Idiopathic (most common).
  • Preterm delivery.
  • Previous breech presentation.
  • Uterine abnormalities, e.g. fibroids and Müllerian duct abnormalities.
  • Placenta praevia and obstructions to the pelvis.
  • Fetal abnormalities.
  • Multiple pregnancy.
97
Q

Consequences of breech presentation

A

Fetal
• Increased risk of hypoxia and trauma in labour.
• Irrespective of the mode of delivery, neonatal and longer-term risks
are increased. The reasons incompletely understood but may be due to:
• association with congenital abnormalities
• many preterm babies are breech at the time of delivery.

Maternal
- Most breeches are delivered by CS.

98
Q

Examination signs that suggests a breech

A

O n examination:
• lie is longitudinal
• head can be palpated at the fundus
• the presenting part is not hard
• the fetal heart is best heard high up on the uterus.
• Ultrasound confirms the diagnosis and should also assess growth and
anatomy because of the association with fetal abnormalities.

99
Q

When, how and why is external cephalic version conducted?

A

Manually turning a breech
or transverse presentation into a cephalic one using US.

From 36wks
in nulliparous women
From 37wks in multiparous ones.

The intention is to
reduce the need for delivery by CS.

100
Q

What needs to occur after ECV

A
  • CTG

- Anti-D if rhesus neg

101
Q

Success rate of ECV

A

50% -efficacy is increased by tocolysis (salbutamol)

102
Q

How safe is ECV?

A

0.5% need CS after due to fetal heart abnormalities or vaginal bleeding

103
Q

Risks of ECV

A
  • pain
  • precipitating labour
  • placental abruption
  • fetomaternal haemorrhage
  • cord accidents
  • CS
104
Q

Natural methods of ECV

A
  • postural
    methods, acupuncture, moxabustion
  • remain unproven.
105
Q

Contraindications to ECV

A 
Absolute
• Caesarean delivery already indicated.
• Antepartum haemorrhage.
• Fetal compromise.
• Oligohydramnios.
• Rhesus isoimmunization.
• Pre-eclampsia.

Relative
• One previous CS.
• Fetal abnormality.
• Maternal hypertension.

106
Q

How are breech babies delivered?

A

Most breech deliveries in the UK, USA, and Europe are by CS, because
meta-analysis of RCTs has shown this to reduce neonatal mortality and
short-term morbidity, although not longer-term morbidity

107
Q

Which breeches are at highest risk of cord prolapse?

A

Footling

108
Q

When might vaginal delivery of breech be most acceptable?

A
  • no compromise
  • <4kg
  • spontaneous onset of labour
  • Extended breech
109
Q

Management of unstable lie

A
  • US
  • Admit from 37 weeks (discharge once stable and longitudinal)
  • CS at 41 weeks if lie not stable
110
Q

Risks of abnormal lie

A
  • Obstructed labour and potential uterine rupture

- Membrane rupture risks cord prolapse

111
Q

Causes of abnormal lie

A
  • Multiparity (particularly >para 2) with lax uterus (common).
  • Polohydramnios.
  • Uterine abnormalities, e.g. fi broids and Müllerian duct abnormalities.
  • Placenta praevia and obstructions to the pelvis.
  • Fetal abnormalities.
  • Multiple pregnancy.
112
Q

Causes of abdo pain in <24weeks

A

1) miscarriage - PV bleeding, +ve test + US
2) Ectopic - brown vaginal bleeding, shoulder tip pain, hCG, US
3) Constipation - lactulose or glycerine sup
4) Round ligament pain - due to stretching. Often bilateral, radiating to the groin and aggrevated by movement
5) UTI - raised nitrites –> abx, increase fluids
6) Fibroid - red degen. conservative treatment, bleeding risk too great for surgery.

113
Q

Why does red degeneration occur?

A

Fibroids often increase in size during pregnancy, disrupting the blood supply to them causing pain

114
Q

Causes of abdo pain >24weeks

A

1) Labour
2) Braxton Hicks contractions - VE = closed cervix. Fibronectin assay if unsure if pre-term. Reassure.
3) Symphysis pubis dysfunction
4) Reflux oesophagitis:
• Exclude pre-eclampsia.
• Antacids, H 2 receptor antagonists.
• Dietary and lifestyle advice
5) Uterine rupture
6) Placental abruption
7) Pre-eclampsia/HELLP

115
Q

RF for uterine rupture

A
  • Previous CS or other uterine surgery.
  • Congenital abnormalities of the uterus.
  • Induction or use of oxytocin in labour.
  • Failure to recognize obstructed labour.
116
Q

Sx uterine rupture

A

• Tenderness over sites of previous uterine scars.
• Fetal parts may be easily palpable.
• Fetus not palpable on VE.
• Vaginal bleeding
• Signs of maternal shock
- CTG may show fetal distress and change in uterine activity (contractions stopping)

117
Q

Mx of uterine rupture

A

Investigations
• F BC.
• Cross-match blood.

Management
• Maternal resuscitation.
• Urgent laparotomy to deliver fetus and repair uterus.

118
Q

Suggest non-pregnancy related causes of abdo pain that one must keep in mind during assessment

A

1) Appendicitis - pain might be RUQ due to belly, fever often absent. FBC, CRP, USS. Diagnostic laparoscopy and appendicectomy.
2) Intestinal obstruction - often due to adhesions. US, ?AXR, drip and suck, ?surgery
3) Acute cholecystitis - progesterone relaxes smooth muscle leading to cholestatis and gallstones. Jaundice if CBD obstruction, raised bili, USS. Tx Conservative - analgesia, anti-emetics, IV fluids, abx and cholecystectomy after delivery
4) Adnexal torsion - more common in pregnancy. Sudden on set abdo pain. US pelvis, doppler (impaired flow). Tx Urgent laparotomy
5) Pancreatitis - more common in pregnancy due to GS. Pain worsened by lying flat, relieved by leaning forward. Lipase, amylase and USS. IV morphine and fluids, NBM. Early surgery as most relapse (Laparoscopic/open cholecystectomy, not ERCP due to the radiation). ITU.
6) lower lobe pneumonia
7) DKA
8) Sickle crisis
9) Domestic abuse

119
Q

5 Causes of intestinal obstruction

A
  • Adhesions.
  • Volvulus.
  • Intussusception.
  • Hernia.
  • Neoplasm.
120
Q

Definition of preterm

A

Birth between 24-37weeks

121
Q

Ratio of spontaneous to indicated pre-term deliveries

A

1/3 medically indicated

2/3 spontaneous

122
Q

Incidence of pre-term

A

5-10%

BUT accounts for 50% of mortalities

123
Q

RF for preterm deliveries

A
  • Previous preterm birth or late miscarriage.
  • Multiple pregnancy.
  • Cervical surgery.
  • Uterine anomalies.
  • Medical conditions, e.g. renal disease.
  • Pre-eclampsia and IUGR (spontaneous and iatrogenic).
124
Q

Presentation of preterm labour

A
  • Due to cervical weakness
  • Associated with infection, inflammation or abruption
  • Abdo pain
  • Contractions
  • SROM
  • Vaginal discharge
  • Mild lower abdo pain
  • Bulging membranes
125
Q

Mx of suspected pre-term

A

History
• Pain/contractions—onset, frequency, duration, severity.
• Vaginal loss: SROM or PV bleeding.
• Obstetric history (check hand-held notes).

Examination
• Maternal pulse, temperature, RR.
• Uterine tenderness (suggests infection/abruption).
• Fetal presentation.
• Speculum: look for blood, discharge, liquor. Takes swabs.
• Gentle VE.
Investigations
• F BC, CRP (raised WCC and CRP suggest infection).
• Swabs, MSU.
• USS for fetal presentation (malpresentation common) and estimated fetal weight (EFW).
• Consider fetal fibronectin/transvaginal USS if available
- if cervix >15mm or fibronectin -ve unlikely to be labour

Tx

  • Consider admitting, inform neonates
  • US for presentaton
  • Steroids - 12mg betamethasone IM OD 2/7
  • IV abx if labour is confirmed
126
Q

How can pre-term delivery be delayed?

A

BV treatment
Progesterone
Cerclage

127
Q

Features suggestive of chorioamnionitis on Hx and Ex

A

History:
• Fever/malaise.
• Abdominal pain, including contractions.
• Purulent/offensive vaginal discharge.

Examination:
• Maternal pyrexia and tachycardia.
• Uterine tenderness.
• Fetal tachycardia.
• Speculum: offensive vaginal discharge—yellow/brown.

Avoid VE as this increases the risk of introducing infection.

128
Q

How should you investigate possible chorioamnionitis?

A
  • FBC, CRP (raised WCC and CRP indicate infection).
  • Swabs (high vaginal swab (HVS), low vaginal swab (LVS)).
  • MSU.
  • USS for fetal presentation, EFW, and liquor volume.
129
Q

Mx of chorioamnionitis

A
  • steroids (betametasone 12mg IM)
  • deliver whatever the gestation
  • broad spectrum antibiotic cover.
130
Q

Mx of PROM

A
  • Exclude chorioamniotis
  • Admit
  • Liaise with SCBU
  • Steroids
  • Abx (erythromycin)
131
Q

Describe the evidence for using abx in PROM

A

ORACLE trial 2001

Infants born to women with preterm, premature rupture of membranes, those whose mothers were randomized to erythromycin experienced a lower incidence of adverse neonatal outcomes and prolongation of pregnancy compared to the placebo group.

132
Q

Which abx should be avoided in PROM and why?

A

Co-amoxiclav is associated with an increased risk of necrotizing enterocolitis
(NEC)

133
Q

Describe the prognosis of PROM

A
  • Dependent on gestation
    <20weeks unlikely to survive
    >22weeks more likely (50%)
    Worse prognosis if spontaneous, better if iatrogenic
134
Q

Risks to fetus of PROM

A
  • Prematurity.
  • Infection.
  • Pulmonary hypoplasia.
  • Limb contractures.
135
Q

Describe the results of the EPICure study

A

Cohort study of babies born in UK + ireland in 1995

<23 weeks 1% survive to discharge and 50% severely disabled

23weeks 11% survive to discharge, 31% severely disabled

24weeks 26% survive to discharge, 24% severely disabled

25 weeks 44% survive to discharge, 22% severely disabled.

136
Q

Definition of prolonged pregnancy

A

FIGO = prolonged pregnancy is defined as any pregnancy that exceeds
42wks (294 days) from the first day of the LMP in a woman with regular
28-day cycles.

137
Q

Incidence of prolonged pregnancy

A

3-10%

  • If previous Hx, incidence rises to 30%, then 40%
138
Q

When can EDD dates not be relied on?

A
  • Uncertainty of LMP (10–30% of women).
  • Irregular periods.
  • Recent use of COCP.
  • Conception during lactational amenorrhea.
139
Q

Risks of prolonged pregnancy

A

Maternal:
- Increased intervention + increased genital trauma

Fetal:
- 4x increase in intrapartum deaths
- 3x increase in early neonatal deaths
- Meconium aspiration + assisted ventilation
- Oligohydramnios
- Macrosomia, shoulder dystocia, and fetal injury.
- Cephalhaematoma.
- Fetal distress in labour.
- Neonatal—hypothermia, hypoglycaemia, polycythaemia, and growth
restriction.
- Postmaturity syndrome

140
Q

Describe post-maturity syndrome

A

= post-term infants with signs of intrauterine malnutrition.

• scaphoid abdomen, little subcutaneous fat on the
body or limbs, peeling skin over the palm and feet, overgrown nails,
and an anxious, alert look.

• Skin stained with meconium.

** Only occurs in a small proportion of babies born after 42wks.

**Can be seen earlier in babies with IUGR.

141
Q

Mx of Prolonged pregnancy

A

1) Confirm EDD accurately
2) Assess RF to indicate induction: Pre-eclampsia, DM, haemorrhage, IUGR
3) Stretch and sweep at 41weeks
4) Induction 41-42 weeks, if declined increase surveillance
5) Daily CTG + report reduction in fetal movements + US + counsel on risks

Oxford handbook O&G (7 decks)

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