WOMEN'S HEALTH - OBSTETRICS Flashcards

1
Q

ECTOPIC PREGNANCY
What is an ectopic pregnancy?

A
  • When a fertilised ovum implants outside of the uterine cavity, 98% tubal
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2
Q

ECTOPIC PREGNANCY
Where is the most common site for an ectopic?
What is the most common site for a ruptured ectopic?

A
  • Ampulla
  • Isthmus
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3
Q

ECTOPIC PREGNANCY
What is the epidemiology of ectopics?
What are some risk factors for ectopics?

A
  • 1 in 100 incidence
  • Previous ectopic (10% recurrence rate), PID, endometriosis, tubal surgery, IUCD, IVF + POP
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4
Q

ECTOPIC PREGNANCY
What are some symptoms of ectopics?

A
  • Amenorrhoea for 6-8w, PV bleeding (small amount, brown)
  • Constant lower abdo (iliac fossa) pain
  • D+V, dizziness + fainting
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5
Q

ECTOPIC PREGNANCY
What are some signs of ectopics?

A
  • Referred shoulder pain due to haemoperitoneum irritating diaphragm
  • Abdo or rebound tenderness
  • Cervical excitation/motion tenderness
  • Peritonism or collapse if rupture
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6
Q

ECTOPIC PREGNANCY
What are some crucial investigations for ectopics?

A
  • Beta-hCG to confirm pregnant – should double every 48h in normal
  • TVS = empty uterus, may show adnexal mass or free fluid
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7
Q

ECTOPIC PREGNANCY
What are some other investigations for ectopics?

A
  • FBC, group + save, serum progesterone <20nmol/L suggests failing pregnancy
  • Laparoscopy gold standard but only used as necessary
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8
Q

ECTOPIC PREGNANCY
What are the 3 management techniques for ectopic pregnancies?

A
  • Expectant
  • Medical
  • Surgical
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9
Q

ECTOPIC PREGNANCY
What is expectant management?
What are the indications?
What indicates that it has worked?

A
  • Effectively do nothing
  • Clinically stable (no Sx), ectopic <35mm, no heartbeat, serum hCG <1000IU/L (consider up to 1500) + able to return for follow up
  • Serum hCG days 2, 4 + 7 (drop ≥15% then repeat weekly until negative)
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10
Q

ECTOPIC PREGNANCY
What is medical management?
What are the indications?
What indicates that it has worked?

A
  • Single dose IM 50mg/m^2 methotrexate
  • No significant pain, unruptured ectopic <35mm, no heartbeat, serum hCG <1500 (consider up to 5000IU/L) + able to return for follow up
  • hCG levels at days 4 + 7 then weekly, <15% fall = ?another dose
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11
Q

ECTOPIC PREGNANCY
What are the requirements for methotrexate management?
What are some side effects?

A
  • Satisfactory liver + renal functions
  • Teratogenic so effective contraception for 3m
  • Conjunctivitis, diarrhoea, abdo pain + stomatitis
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12
Q

ECTOPIC PREGNANCY
What surgical management is offered?
What are indications?
What else should be given?

A
  • Salpingectomy or salpingotomy
  • Does not meet expectant or medical criteria (>35mm, visible heartbeat, ruptured)
  • Anti-D for rhesus -ve in surgical management
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13
Q

ECTOPIC PREGNANCY
How do you choose which type of surgical management to give?

A
  • Salpingectomy if contralateral tube + ovary healthy to reduce recurrence
  • Salpingotomy if contralateral tube defected
  • Laparoscopy preferred to laparotomy unless haemodynamically unstable
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14
Q

MISCARRIAGE
What is a miscarriage?

A
  • Spontaneous termination of a pregnancy before 24w gestation
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15
Q

MISCARRIAGE
What is the epidemiology of miscarriage?

A
  • 15–20% of pregnancies with 85% in first trimester
  • No increased risk of having another miscarriage after 1 but is after 2
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16
Q

MISCARRIAGE
What are the 6 types of miscarriage?

A
  • Threatened
  • Inevitable
  • Incomplete
  • Complete
  • Missed
  • Septic
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17
Q

MISCARRIAGE
What are the most common causes of miscarriage in first trimester?

A

Chromosome abnormality –
- Autosomal trisomy most common (trisomy 16)
- Most common single chromosomal anomaly is 45X
- Increasing maternal age biggest risk

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18
Q

MISCARRIAGE
What is the most common cause of miscarriage in the second trimester?

A
  • Incompetent cervix
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19
Q

MISCARRIAGE
What are some other causes of miscarriage?

A
  • PCOS
  • TORCH infections
  • Iatrogenic (amniocentesis, CVS)
  • Smoking, substance abuse
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20
Q

MISCARRIAGE
What are some risk factors for miscarriage in the second trimester?

A

Previous cervical surgery, BV in 2nd trimester

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21
Q

MISCARRIAGE
What is a threatened miscarriage?

A
  • Foetus alive but miscarriage may occur (majority don’t)
  • Painless vaginal bleeding with closed cervical os
  • TVS = viable intrauterine pregnancy
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22
Q

MISCARRIAGE
What is an inevitable miscarriage?

A
  • Miscarriage will occur
  • Heavy PV bleed with clots + crampy abdo pain with open cervical os (1 finger)
  • POC not passed
  • TVS = intrauterine gestation sac, foetus may be alive but miscarriage imminent
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23
Q

MISCARRIAGE
What is an incomplete miscarriage?

A
  • Not all POC been passed
  • PV bleed, abdo pain + open cervical os with POC in canal
  • Medical or surgical mx as infection risk
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24
Q

MISCARRIAGE
What is a complete miscarriage?

A
  • Full miscarriage occurred with all foetal tissue passing
  • Bleeding + pain cease, uterus no longer enlarged, cervical os closed
  • TVS = empty uterus, endometrial thickening <15mm, exclude ectopic
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25
Q

MISCARRIAGE
What is a missed miscarriage?

A
  • Foetus not developed or died in utero but this is not recognised until bleeding occurs or TVS
  • TVS - non-viable intrauterine pregnancy (smaller than expected) e.g. 12w scan shows 9w foetus with no heartbeat
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26
Q

MISCARRIAGE
What is a blighted ovum?

A
  • In missed miscarriage, a gestational sac >25mm but no embryonic/foetal pole
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27
Q

MISCARRIAGE
What is a septic miscarriage?

A
  • Contents of uterus infected causing endometritis
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28
Q

MISCARRIAGE
What is a pregnancy of uncertain viability?

A

Small sac with no visible heartbeat,
rescan 10–14d

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29
Q

PREGNANCY OF UNKNOWN LOCATION
What is a pregnancy of unknown location?

A

No sign of intrauterine, ectopic or retained POC but positive beta-hCG

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30
Q

PREGNANCY OF UNKNOWN LOCATION
What is the management of pregnancy of unknown location?

A
  • Beta-hCG >1500IU/L ?ectopic
  • Significant distress = laparoscopy
  • Stable = repeat beta-hCG after 48h
  • If no Dx after 3 samples = expectant or methotrexate Mx
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31
Q

MISCARRIAGE
What are the generalised investigations and management of miscarriage?

A
  • Refer to EPAU for Ix
  • Speculum exam = cervical os open/closed, remove POC if in cervical os
  • Serum beta-hCG levels
  • TVS = location + viability
  • Histological exam of any tissue passed vaginally
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32
Q

MISCARRIAGE
What would serum beta-hCG levels show in miscarriage?

A
  • Serial testing as should double every 48h for first few weeks of pregnancy
  • Levels may be less than expected for dates
  • Falling indicates failing pregnancy
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33
Q

MISCARRIAGE
What is the first line management of miscarriage?
What are the indications?
What is the follow up?

A
  • Expectant (wait 7–14d)
  • <6w, not bleeding heavily, no signs of infection
  • Urinary beta-hCG after 3w or repeat TVS if persistent or worse bleeding (or not started)
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34
Q

MISCARRIAGE
What is the medical management of a miscarriage?
What is the follow up?

A
  • PV/PO synthetic prostaglandin misoprostol
  • Contact HCP if no bleeding in 24h
  • Urinary beta-hCG 3w after to exclude ectopic or molar
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35
Q

MISCARRIAGE
What are the risks of expectant and medical management?

A
  • Bleeding continuing
  • Increased pain
  • Infected POC
  • Failure
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36
Q

MISCARRIAGE
What are some indications for surgical management?

A
  • Heavy bleeding
  • Infection
  • Failed other methods
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37
Q

MISCARRIAGE
What are the options for surgical management?

A
  • Vacuum aspiration (suction curettage) under local as OP
  • Surgical Mx (evacuation of retained products of conception) under general
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38
Q

MISCARRIAGE
What else may be given in the management of miscarriage?

A
  • Anti-D to rhesus -ve women if >12w, heavily bleeding or surgical Mx
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39
Q

MISCARRIAGE
What is a recurrent miscarriage?

A
  • ≥3 consecutive miscarriages in the first trimester with the same biological father
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40
Q

MISCARRIAGE
What are some causes of recurrent miscarriage?

A
  • Antiphospholipid syndrome
  • Hereditary thrombophilias (Factor V leiden deficiency, factor II prothrombin gene mutation, protein C/S deficiency)
  • Uterine abnormalities (uterine septate, fibroids)
  • Poor controlled chronic conditions (DM, thyroid, SLE)
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41
Q

MISCARRIAGE
What is antiphospholipid syndrome?

A
  • Hypercoaguable state presenting with thrombosis + pregnancy issues (recurrent miscarriage)
  • Associated with antiphospholipid antibodies
  • Can occur on own or secondary to SLE
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42
Q

MISCARRIAGE
What is the management of antiphospholipid syndrome?

A

Low dose aspirin + LMWH

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43
Q

MISCARRIAGE
What are the investigations for recurrent miscarriage?

A

≥3 1st trimester, ≥1 in 2nd –
- Lupus anticoagulant, anti-cardiolipin + phospholipid antibodies
- Thrombophilia screen
- Pelvic USS for structural issues
- Cytogenic analysis of POC after 3rd miscarriage
- Parental blood for karyotyping

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44
Q

TERMINATING PREGNANCY
What is the legal framework for terminating pregnancies?

A
  • 1967 Abortion Act (+ 1990 amendment which reduced gestation from 28 to 24w)
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45
Q

TERMINATING PREGNANCY
What are the requirements for an abortion?

A
  • <24w
  • Continuing pregnancy = great risk to physical or mental health of woman or existing children in family (clinical judgement)
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46
Q

TERMINATING PREGNANCY
When may an abortion be performed after 24w?

A
  • Continuing is likely to risk mother’s life
  • Prevents grave injury to physical or MH of woman
  • Substantial risk of serious handicap for baby
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47
Q

TERMINATING PREGNANCY
What are the legal requirements for an abortion?

A
  • 2 registered medical practitioners must sign to agree indication
  • Must be registered medical practitioner in an approved premise
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48
Q

TERMINATING PREGNANCY
What is some pre-abortion care?

A
  • Marie Stopes UK charity that provides abortion services (remote service if <10w gestation, phone consultation, meds issued remotely to take at home)
  • Women should be offered counselling
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49
Q

TERMINATING PREGNANCY
What is the medical management of abortion?

A
  • More appropriate in earlier pregnancy, <24w, <10w can be done at home
  • Mifepristone (anti-progesterone) to halt pregnancy + relax cervix
  • Misoprostol (prostaglandin analogue) 24-48h after for contractions
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50
Q

TERMINATING PREGNANCY
What is done before surgical management of abortion?

A
  • Cervical priming with mifepristone, misoprostol or osmotic dilators (>14w insert into cervix + gradually expand as absorb fluid to open cervical canal)
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51
Q

TERMINATING PREGNANCY
What is the surgical management of abortion?

A
  • Cervical dilatation + vacuum aspiration of uterus contents <14w
  • Cervical dilatation + evacuation using forceps >14w
  • Rh -ve >10w = anti-D
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52
Q

TERMINATING PREGNANCY
What is post-abortion care?

A
  • Pregnancy test at 3w
  • Contraception advice
  • Complications = infection (#1), bleeding, pain, failure or damage to genital tract
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53
Q

HYPEREMESIS
How common is nausea and vomiting in pregnancy?

A
  • Very, particularly early on starts in early first trimester, peaks 8–12w + resolves 16–20w
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54
Q

HYPEREMESIS
What is believed to be responsible for N+V in pregnancy?

A
  • Placental beta-hCG
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55
Q

HYPEREMESIS
When is N+V worse?

A

more severe in molar + multiple pregnancies where beta-hCG high

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56
Q

HYPEREMESIS
What are some associations of hyperemesis gravidarum?

A
  • nulliparity,
  • hyperthyroid,
  • obesity,
  • decreased in smokers
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57
Q

HYPEREMESIS
What is the clinical presentation of hyperemesis gravidarum?

A
  • Severe + excessive N+V
  • Associated with dehydration, ketosis + weight loss
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58
Q

HYPEREMESIS
What are the complications?

A

May lead to complications like Mallory-Weiss tear

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59
Q

HYPEREMESIS
What is the diagnostic triad for hyperemesis gravidarum?

A

Triad –
- >5% weight loss compared to before pregnancy
- Dehydration
- Electrolyte imbalance

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60
Q

HYPEREMESIS
How is severity assessed?

A

Pregnancy-Unique Quantification of Emesis (PUQE) –
- <7 mild,
- 7-12 mod,
- >12 severe

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61
Q

HYPEREMESIS
What are some investigations for hyperemesis gravidarum?

A
  • Urine dipstick for ketones, MSU to exclude UTI
  • FBC (raised haematocrit)
  • U+Es (electrolyte imbalances + dehydration)
  • May have hypochloraemic metabolic alkalosis
  • Higher beta-hCG levels
  • USS to reassure + exclude multiple/molar
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62
Q

HYPEREMESIS
What would warrant hospital or EPAU admission?

A
  • Unable to tolerate PO antiemetics or fluids
  • > 5% weight loss compared to before pregnancy
  • Ketones present in dipstick (++ significant)
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63
Q

HYPEREMESIS
What is the inpatient management of hyperemesis gravidarum?

A
  • Monitor U+Es
  • NBM until tolerate PO = IV fluids + anti-emetics
  • Vitamin supplements (incl. thiamine), may need artificial nutrition to prevent Wenicke-Korsakoff
  • Thromboprophylaxis with TED stockings + LMWH
  • Small + frequent meals when eating allowed
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64
Q

HYPEREMESIS
What is the community management of hyperemesis gravidarum?

A
  • 1st line antiemetic = promethazine or cyclizine (anti-histamines)
  • 2nd line = ondansetron (5-HT3 antagonist) or metoclopramide (dopamine antagonist)
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65
Q

HYPEREMESIS
What alternative management can be used?

A

Complementary therapies like ginger or wrist acupressure

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66
Q

ANTENATAL APPTS
In terms of antenatal care…

i) who is in charge of low risk pregnancies?
ii) high risk pregnancies?
iii) how many visits?
iv) what would you do if reduced foetal movements?

A

i) Midwife-led with GP input
ii) Doctor/consultant led with midwives alongside
iii) 10 if nulliparous, subsequent 7
iv) Handheld doppler for heartbeat – USS if not heard, CTG if present

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67
Q

ANTENATAL APPTS
Define…

i) gestational age
ii) estimated date of delivery
iii) gravidity
iv) parity

A

i) duration of pregnancy starting from date of LMP
ii) 40w gestation
iii) Total # of pregnancies
iv) number of births ≥24w regardless of outcome

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68
Q

ANTENATAL APPTS
When is the first visit?
What is done?

A

Booking 8–12w –
- General info (diet, alcohol, smoking, folic acid + vitamin D advice, antenatal classes, family origin questionnaire
- FBC, blood group, rhesus status, haemoglobinopathies
- HIV, hep B + syphilis screening offered
- Urine MC&S for asymptomatic bacteriuria

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69
Q

ANTENATAL APPTS
What is the recommended amount of folic acid?

A
  • ALL 400mcg
  • 5mg if – AEDs, coeliac, DM, >30kg/m^2, NTD risk
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70
Q

ANTENATAL APPTS
When is the dating scan done?
What happens?

A

11–13+6w –
- Confirm viability
- Singleton/multiple
- Estimate gestational age with crown rump length (top of head > bottom of buttocks)
- Detect major structural abnormalities like anencephaly
- Offer combined test

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71
Q

ANTENATAL APPTS
When is the anomaly scan?
What happens?

A

18–20+6w –
- Detect major abnormalities (NTD, CHD, CNS abnormality, renal agenesis)
- Around 20w foetal movements start + continue (refer if none by 24w)

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72
Q

ANTENATAL APPTS
After the anomaly scan, routine care is given but at what times?

A
  • 25w (primis)
  • 28w (all)
  • 31w (primis)
  • 34w (all)
  • 36w (all)
  • 38w (all)
  • 40w (primis)
  • 41w (all)
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73
Q

ANTENATAL APPTS
What routine care is given at 25w for primis?

A
  • BP, urine dipstick, symphysis-fundal height (after 20w should correlate to gestational age ± 2cm)
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74
Q

ANTENATAL APPTS
What routine care is given at 28w?

A
  • BP, urine dipstick, SFH
  • OGTT if risk factors for GDM
  • Second screen for anaemia (FBC), blood group + rhesus status
  • First dose of anti-D prophylaxis if Rh-ve
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75
Q

ANTENATAL APPTS
What routine care is given at…

i) 31w (primis)?
ii) 34w?
iii) 36w?

A

i) BP, urine dipstick, SFH
ii) BP, urine dipstick, SFH + second dose of anti-D if Rh-ve
iii) BP, urine dipstick, SFH, check presentation (?ECV), info about breastfeeding, vitamin K + baby blues

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76
Q

ANTENATAL APPTS
What routine care is given at…

i) 38w?
ii) 40w (primis)?
iii) 41w?

A

i) BP, urine dipstick, SFH
ii) BP, urine dipstick, SFH, discuss options for prolonged pregnancy
iii) BP, urine dipstick, sFH, discuss induction

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77
Q

ANTENATAL SCREENING
What pre-test information should be provided before antenatal screening?

A
  • Conditions screened for
  • When + how test carried out
  • How reliable test is
  • What results mean + options
  • False +ve/-ve + detection rates
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78
Q

ANTENATAL SCREENING
What are the 3 main syndromes screened for in pregnancy?

A
  • Patau’s (trisomy 13)
  • Edward’s (trisomy 18)
  • Down’s (trisomy 21)
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79
Q

ANTENATAL SCREENING
What screening is offered in early pregnancy and when?

A

Combined test (11–13+6w) –
- Nuchal translucency (thickness of back of foetus’ neck on USS)
- Beta-hCG
- Pregnancy associated plasma protein-A (PAPP-A)

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80
Q

ANTENATAL SCREENING
What results indicate higher risk for…

i) nuchal translucency?
ii) beta-hCG?
iii) PAPP-A?

What else is taken into account?

A

i) >6mm
ii) Higher result
iii) Lower result

  • Maternal age, USS crown rump length, detection rate 85%
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81
Q

ANTENATAL SCREENING
What screening is offered if the mother is too late for the combined test and when?

A

Triple or quadruple test 15–20w but only tests for Down’s syndrome –
- Beta-hCG
- Alpha-fetoprotein
- Oestriol
- Inhibin (quadruple)

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82
Q

ANTENATAL SCREENING
What results indicate higher risk for…
i) beta-HCG?
ii) AFP?
iii) oestriol?
iv) inhibin?

A

i) Higher result
ii) Lower result
iii) Lower result
iv) Higher result

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83
Q

ANTENATAL SCREENING
What risk score would warrant further invasive tests?
What are those tests?

A
  • > 1:150 = screen +ve
  • Amniocentesis
  • Chorionic villus sampling (CVS)
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84
Q

AMNIOCENTESIS
What is amniocentesis?

A

It involves aspiration of amniotic fluid which contains foetal cells shed from the skin and gut.
It is performed transabdominally with ultrasound guidance.

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85
Q

AMNIOCENTESIS
When is amniocentesis performed?

A

from 15 weeks onwards

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86
Q

AMNIOCENTESIS
What are the indications for amniocentesis?

A

o For karyotyping if screening tests suggest aneuploidy.
o DNA analysis if parents are carriers of an identifiable mutation, like CF or thalassaemia.
o For enzyme assays looking for inborn errors of metabolism.
o For diagnosis of fetal infections such as CMV and toxoplasmosis.

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87
Q

AMNIOCENTESIS
What are the benefits of amniocentesis?

A

o Lower procedure-attributed miscarriage rate than CVS (71%).
o Less risk of maternal contamination or placental mosaicism

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88
Q

AMNIOCENTESIS
What are the risks of amniocentesis?

A

o Miscarriage (1%)
o Failure to culture cells
o Full karyotyping may take 3wks.

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89
Q

CHORIONIC VILLUS SAMPLING
What is chorionic villus sampling?

A

Involves aspiration of some trophoblastic cells from the placenta under USS guidance.
It is used for karyotyping
Is usually performed transabdominally, occasionally transcervically.

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90
Q

CHORIONIC VILLUS SAMPLING
when is chorionic villus sampling performed?

A

Usually between 10-13 weeks

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91
Q

CHORIONIC VILLUS SAMPLING
what are the indications for chorionic villus sampling?

A

o For karyotyping if 1st trimester screening test suggests high risk for aneuploidy.
o For DNA analysis if parents are carriers of an identifiable gene mutation such as cystic fibrosis or thalassaemia.

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92
Q

CHORIONIC VILLUS SAMPLING
what are the benefits of chorionic villus sampling?

A

Allows 1st trimester TOP if an abnormality is detected:
o Can be performed surgically.
o Can be done before the pregnancy has become physically apparent.

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93
Q

CHORIONIC VILLUS SAMPLING
what are the risks of chorionic villus sampling?

A

o Miscarriage as a result of CVS is estimated at 1%.
o Increases risk of vertical transmission of blood-borne viruses such as HIV and hepatitis B.
o False negative results (rare) from contamination with maternal cells—especially with DNA
analysis requiring PCR.
o Placental mosaicism producing misleading results—estimated at <1%.

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94
Q

ANTENATAL SCREENING
What other testing is available in the private sector?
What does it involve?

A
  • Non-invasive prenatal testing
  • Analyses fragments of foetal DNA in maternal blood
  • 99% accurate, done from 10w
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95
Q

APH
What is an antepartum haemorrhage (APH)?

A
  • Genital tract bleeding after 24w gestation
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96
Q

APH
What are the causes of APH?

A

Majority idiopathic, dangerous causes –
- Placental abruption or praevia
- Vasa praevia
- Morbidly adherent placenta

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97
Q

APH
What are some generic investigations for APH?

A
  • Exclude placenta praevia with USS
  • Kleihauer test to confirm transplacental blood loss from foetus>mother
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98
Q

APH
What are some complications of APH?

A
  • PPH, DIC
  • Premature labour
  • ITU admission
  • Maternal or foetal death
  • Sheehan’s syndrome
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99
Q

PLACENTA PRAEVIA
What is placenta praevia?

A
  • When placenta is inserted wholly, or in part, into the lower segment of the uterus (low lying placenta)
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100
Q

PLACENTA PRAEVIA
What are the grades of placenta praevia?

A

Minor (I or II) –
- I = reaches lower segment but not internal os
- II = reaches internal os but doesn’t cover
Major (III or IV) –
- III = covers internal os before dilation (not when dilated)
- IV = completely covers internal os
- Cervical effacement + dilation > catastrophic bleeding + potential maternal + foetal death

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101
Q

PLACENTA PRAEVIA
What are some risk factors for placenta praevia?

A
  • Embryos more likely to implant on lower segment scar from previous c-section
  • Multiple pregnancy
  • Multiparity
  • Previous praevia
  • Assisted conception
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102
Q

PLACENTA PRAEVIA
What is the clinical presentation of placenta praevia?

A
  • PAINLESS PV bleeding, BRIGHT RED blood, shock IN proportion to visible loss
  • Foetus may have abnormal lie + presentation (breech + transverse)
  • Uterus is not tender
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103
Q

PLACENTA PRAEVIA
What are the investigations for placenta praevia?

A
  • TV USS safe + more accurate
  • Can be Dx on routine antenatal USS (20w)
  • Repeat USS at 36w if minor or 32w if major
  • If over or close to internal os repeat scans every 2w
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104
Q

PLACENTA PRAEVIA
What are some complications of placenta praevia?

A
  • PPH
  • Placenta accreta or percreta
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105
Q

PLACENTA PRAEVIA
What is the normal management of placenta praevia?

A
  • Asymptomatic can stay at home if access to hospital, aware of risks/Sx, companion (rest + avoid intercourse)
  • <20mm from os = elective c-section ≥38w or earlier if bleeding does not settle
  • Anti-D if Rh-ve
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106
Q

PLACENTA PRAEVIA
What is the acute management of placenta praevia?

A
  • ABCDE + admission
  • IV access, fluids (crystalloid), X-match blood, inform senior team + paeds
  • Foetal monitoring with CTG ± delivery
  • Steroids if <34w gestation
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107
Q

PLACENTAL ABRUPTION
What is placental abruption?

A
  • Placenta prematurely separates (in part or fully) from uterus wall leading to APH from where the placenta was previously attached
  • Blood can accumulate behind placenta in uterine cavity or exit via cervix
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108
Q

PLACENTAL ABRUPTION
What are the major risk factors for placental abruption?
What are some other risk factors?

A
  • IUGR, pre-eclampsia or pre-existing HTN, maternal smoking + previous abruption
  • Cocaine use, multiple pregnancy or high parity, trauma
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109
Q

PLACENTAL ABRUPTION
What are the 2 types of abruption?

A
  • Concealed = cervical os closed so haemorrhage remains in uterus
    – Maternal shock out of proportion with visible loss may > underestimation
  • Revealed = PV bleeding
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110
Q

PLACENTAL ABRUPTION
What is the clinical presentation of placental abruption?

A
  • Sudden onset severe abdo PAIN which is continuous
  • PV bleeding often DARK red
  • Maternal shock (hypotension, tachycardia = adverse signs)
  • Foetal distress common on CTG (absent or abnormal FHR)
  • Posterior placenta may cause severe backache
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111
Q

PLACENTAL ABRUPTION
What are some investigations for placental abruption?

A
  • Tender “woody” uterus on palpation (blood invading myometrium)
  • FBC, coagulation, X-match (may need catheter for urine output + U+Es for renal function)
  • USS + CTG for foetal wellbeing + exclude praevia
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112
Q

PLACENTAL ABRUPTION
What are the maternal and foetal complications of placental abruption?

A
  • Shock, DIC, renal failure, PPH
  • IUGR, hypoxia + death
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113
Q

PLACENTAL ABRUPTION
What is the general management of placental abruption?

A
  • Mum + foetus stable at <36w then admit + observe carefully, induce after 36w with amniotomy aiming for vaginal delivery, steroids if <34w
  • Anti-D if Rh-ve
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114
Q

PLACENTAL ABRUPTION
What is the management of acute placental abruption?

A
  • A–E resus
  • IV access, fluids, ABO Rh compatible or O-ve blood
  • Mum unstable, foetal distress or heavy bleeding = emergency c-section
  • Steroids if <34w
    MUM COMES FIRST
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115
Q

ADHERED PLACENTA
What is a morbidly adhered placenta?

A
  • The chorionic villi attach to the myometrium rather than being restricted within the decidua basalis
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116
Q

ADHERED PLACENTA
What are the different types of morbidly adhered placenta?

A
  • Accreta = placenta invades into superficial myometrium
  • Increta = placenta invades deeper through the myometrium
  • Percreta = placenta invades through myometrium, into nearby organs of abdomen (bladder, bowel)
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117
Q

ADHERED PLACENTA
What are some risk factors for a morbidly adhered placenta?

A
  • Previous c-sections (placenta attaches to site)
  • Myomectomy
  • Surgical TOP
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118
Q

ADHERED PLACENTA
What are some investigations for a morbidly adhered placenta?

A
  • USS may show loss of definition between wall of uterus + abnormal vasculature
  • MRI scan if degree of adherence uncertain
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119
Q

ADHERED PLACENTA
What are some complications of a morbidly adhered placenta?

A
  • Poor placental separation may occur > difficult to deliver placenta after baby delivered > retained products > infection risk
  • Delivery risks = PPH, transfusion, caesarean hysterectomy, ITU
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120
Q

ADHERED PLACENTA
What is the management of a morbidly adhered placenta?

A
  • Elective LSCS at 36–37w
  • ?Caesarean hysterectomy
  • ?Leave in situ (expectant)
  • ?Uterus preserving surgery (resecting part of myometrium + placenta)
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121
Q

ADHERED PLACENTA
What is the acute management of a morbidly adhered placenta?

A
  • Blood + blood products available
  • Local ITU availability
  • Tamponade with balloon
  • Hysterectomy last resort
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122
Q

VASA PRAEVIA
What is vasa praevia?

A
  • Major foetal vessels run in membranes below the presenting foetal part, so they present before the foetus, unsupported by placental tissue or umbilical cord
  • Exposed mean prone to rupture + bleed
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123
Q

VASA PRAEVIA
What are some risk factors for vasa praevia?

A
  • Placenta praevia
  • Multiple pregnancy
  • IVF pregnancy
  • Bilobed placentas
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124
Q

VASA PRAEVIA
What is the clinical presentation of vasa praevia?

A
  • PV bleed straight after rupture of foetal membranes > rapid foetal distress
  • CTG abnormalities (bradycardia) with high foetal mortality
  • No major maternal risk just major foetal risk (massive haemorrhage)
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125
Q

VASA PRAEVIA
What is the management of vasa praevia?

A
  • A–E approach, manage bleeding
  • Deliver c-section (elective if antenatally diagnosed, emergency if present with bleeding)
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126
Q

PRE-ECLAMPSIA
What is pre-eclampsia?

A
  • Pregnancy induced HTN + proteinuria at >20w gestation
  • Results due to abnormal development of the placenta
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127
Q

PRE-ECLAMPSIA
How can pre-eclampsia be classified?

A
  • Mild-mod = pre-eclampsia without severe HTN (<160/110) and NO Sx, biochemical or haematological impairment
  • Severe = pre-eclampsia w/ severe HTN ± Sx ± biochem ± haem impairment
  • Early <34w, late >34w
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128
Q

PRE-ECLAMPSIA
What is the normal physiology of the placenta?

A
  • Spiral arteries dilate + develop into large utero-placental arteries, supplying lots of blood to the endometrium > placenta + foetus
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129
Q

PRE-ECLAMPSIA
What is the pathophysiology of pre-eclampsia?

A
  • Spiral arteries do not remodel + dilate but become fibrous so utero-placental arteries deliver less blood > placental ischaemia
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130
Q

PRE-ECLAMPSIA
What is the result of placental ischaemia?

A
  • Pro-inflammatory protein + thromboplastin release leads to endothelial damage > vasoconstriction, clotting dysfunction + increased vascular permeability
  • Ultimately leads to poor renal perfusion > RAAS activation > HTN, proteinuria ± oedema > pre-eclampsia + eclampsia (if continues)
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131
Q

PRE-ECLAMPSIA

What are the…

i) high risk
ii) moderate risk

factors for pre-eclampsia?

A

i) Pre-existing HTN, previous pre-eclampsia, CKD, autoimmune (SLE, T1DM)
ii) Nulliparity, multiple pregnancy, >10y pregnancy interval, FHx, >40y, BMI >35kg/m^2

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132
Q

PRE-ECLAMPSIA
What are the 2 main causes of symptoms in pre-eclampsia?

A
  • Local areas of vasospasm leading to hypoperfusion
  • Oedema due to increased vascular permeability + hypoproteinaemia
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133
Q

PRE-ECLAMPSIA
What symptoms are caused by local areas of vasospasm and what area is affected?

A

Renal = glomerular damage (low GFR) –
- Oliguria + proteinuria
Retinal –
- Visual disturbances (blurred, flashing lights, scotoma)
Liver = injury + swelling stretches liver capsule –
- RUQ or epigastric pain

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134
Q

PRE-ECLAMPSIA
What symptoms are caused by oedema?

A
  • Face, hands + legs (generalised)
  • SOB + cough (pulmonary)
  • Headaches, confusion + seizures in eclampsia (cerebral)
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135
Q

PRE-ECLAMPSIA
What are the signs of pre-eclampsia?

A
  • Raised BP + proteinuria are hallmarks
  • Rapid weight gain, RUQ tenderness
  • Ankle clonus (brisk reflexes normal in pregnancy but not clonus)
  • Papilloedema if severe
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136
Q

PRE-ECLAMPSIA
How can a diagnosis of pre-eclampsia be made?

A
  • BP ≥140/90mmHg
  • Proteinuria in a 24h collection (>0.3g) or dipstick with +
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137
Q

PRE-ECLAMPSIA
What blood investigations would you do in pre-eclampsia?

A
  • FBC with platelets (thrombocytopenia)
  • Serum uric acid levels (raised due to renal issues)
  • LFTs (elevated liver enzymes ALT + AST)
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138
Q

PRE-ECLAMPSIA
What other investigations could you perform in pre-eclampsia?

A
  • Proteinuria on dipstick (++ or +++ is severe)
  • Protein:Creatinine ratio (PCR) ≥30ng/nmol = significant proteinuria
  • Accurate dating + USS to assess foetal growth
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139
Q

PRE-ECLAMPSIA
What are the 2 big complications of pre-eclampsia?

A
  • Eclampsia
  • HELLP syndrome
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140
Q

PRE-ECLAMPSIA
What is eclampsia?
What causes it?

A
  • Generalised tonic-clonic seizures in a patient with a Dx of pre-eclampsia
  • Hypoalbuminaemia > hypovolaemia > cerebral hypoperfusion
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141
Q

PRE-ECLAMPSIA
What is the management of eclampsia?

A

IV magnesium sulfate to prevent + treat seizures –
- Reduces DIC risk as reduced platelet aggregation
- Continue 24h after last seizure or delivery
Treat HTN with labetalol 1st line or nifedipine
Stabilise mum and delivery baby

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142
Q

PRE-ECLAMPSIA
What needs to be monitored when giving magnesium sulfate?

A
  • Magnesium levels for toxicity
  • Reduced reflexes, confusion + respiratory depression
  • Calcium gluconate first line
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143
Q

HELLP
What is HELLP syndrome?

A

HELLP syndrome is a subtype of severe pre-eclampsia characterized by
- hemolysis (H),
- elevated liver enzymes (EL),
- low platelets (LP).

Usually occurs within 7 days of delivery.

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144
Q

HELLP
How does HELLP syndrome present?

A

➢ Nausea/vomiting
➢ Hypertension
➢ Brisk tendon reflexes
➢ RUQ/Epigastric pain
➢ General malaise/headache
➢ Oedema/bleeding
➢ Visual problems, jaundice

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145
Q

HELLP
what other condition is HELLP associated with?

A
  • 10% have antiphospholipid syndrome
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146
Q

HELLP
what are the risk factors for HELLP?

A

➢ White ethnicity
➢ Maternal age >35 yrs.
➢ Obesity
➢ Chronic hypertension
➢ DM
➢ Autoimmune disorders
➢ Abnormal placentation and multiple gestation
➢ Previous pregnancy with preeclampsia

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147
Q

HELLP
what are the investigations for HELLP?

A

➢ FBC with platelets: hemolysis,
elevated LFT, low platelets
➢ Peripheral blood smear, serum LDH, uric acid
➢ LFT, Bilirubin
➢ Fetal ultrasound

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148
Q

HELLP
what is the management for HELLP?

A

➢ Seizure prophylaxis (magnesium sulfate), IV dexamethasone, labetalol. IM beclametasone
when patient <36wks
➢ Delivery is definitive treatment (should be done when patient is 37+ wks)

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149
Q

PRE-ECLAMPSIA
What are some other important complications of pre-eclampsia?

A
  • DIC, CVA (haemorrhagic)
  • Multi-organ failure (renal, hepatic)
  • Foetus = IUGR (poorly perfused placenta), prematurity, placental abruption
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150
Q

PRE-ECLAMPSIA
What should be given to women who are at high or moderate risk of pre-eclampsia and why?

A
  • 75mg aspirin PO OD at 12w until birth
  • Spiral arteries form around 12w so thought to help them develop
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151
Q

PRE-ECLAMPSIA
What medical treatment can be given for pre-eclampsia?

A

Treat HTN with –
- PO Labetalol first line (can use IV if severe + inpatient)
- PO nifedipine (used if asthmatic)
- Hydralazine too
- ACEi = CONTRAINDICTAED

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152
Q

PRE-ECLAMPSIA
What is the criteria for outpatient management of pre-eclampsia?
What care is given?

A
  • BP <160/110, no or low proteinuria (≤+, <0.3g/24h) + no symptoms
  • Weekly review of bloods, twice weekly mother + foetal evaluation (HBPM + urine)
  • Any changes > hospital
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153
Q

PRE-ECLAMPSIA
What is the definitive cure of pre-eclampsia?
What are the indications?
What method is preferred?

A
  • Delivery (around 36w)
  • Mother = liver/renal failure, HELLP, eclampsia, severe Sx
  • Foetal = severe IUGR, oligohydramnios, abnormal CTG
  • PV + neuraxial techniques for spinal/epidural preferred
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154
Q

PRE-ECLAMPSIA
What is the management of pre-eclampsia during delivery?

A
  • Regular investigations (BP, urinalysis, bloods, CTG, fluid balance chart (restrict if severe)
  • BP control (IV labetalol first line of nifedipine if asthmatic)
  • IV magnesium sulfate prophylaxis during labour + 24h after
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155
Q

PRE-ECLAMPSIA
What are the 3 other types of HTN in pregnancy conditions?

A
  • Chronic HTN
  • Gestational/pregnancy induced HTN
  • Pre-eclampsia superimposed on chronic HTN
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156
Q

PRE-ECLAMPSIA
What is chronic HTN?

A
  • HTN diagnosed prior to pregnancy, before 20w gestation or that develops during pregnancy but does not resolve postpartum
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157
Q

PRE-ECLAMPSIA
What is gestational or pregnancy induced HTN?

A
  • New HTN >20w gestation with NO proteinuria that resolves after giving birth
  • 25% will progress to pre-eclampsia
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158
Q

PRE-ECLAMPSIA
What is pre-eclampsia superimposed on chronic HTN?

A
  • HTN + no proteinuria <20w with new onset proteinuria after 20w
  • HTN + proteinuria <20w with sudden rise in proteinuria or BP when HTN was well controlled, or development of thrombocytopenia or abnormal ALT/AST
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159
Q

IUGR
What is intrauterine growth restriction (IUGR)?

A
  • Baby has not maintained its growth potential (slows or creases)
  • I.e. drops below centile line it was following > pathological
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160
Q

IUGR
What are the two types of IUGR?

A
  • Symmetrical = entire body is proportionately small, tends to be seen in early onset IUGR, TORCH + chromosomal abnormalities
  • Asymmetrical = undernourished foetus that is compensating by directing most of its energy to maintain growth of vital organs like brain + heart
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161
Q

IUGR
What might be seen in asymmetrical IUGR?

A

Head-sparing effect –
- Normal head size but small abdominal circumference + thin limbs
- Mostly secondary to placental insufficiency

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162
Q

IUGR
What is small for gestational age (SGA)?

A
  • Estimated foetal weight (EFW) or abdominal circumference (AC) below 10th centile for their gestational age
  • May be constitutionally small with no pathology identified (parental height)
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163
Q

IUGR
What is low birth weight?

A
  • Baby born with a weight <2.5kg (regardless of gestational age)
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164
Q

IUGR
What are the 3 broad categories causing IUGR?

A
  • Placental insufficiency (most common cause)
  • Maternal factors
  • Foetal factors
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165
Q

IUGR
What are some placental causes of IUGR?

A
  • Abnormal trophoblast invasion (pre-eclampsia, placenta accreta)
  • Infarction, abruption, location (praevia)
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166
Q

IUGR
What are some maternal causes of IUGR?

A
  • Chronic disease (HTN, cardiac, CKD)
  • Substance abuse (cocaine, alcohol) smoking, previous SGA baby
  • Autoimmune
  • Low socioeconomic status
  • > 40
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167
Q

IUGR
What are some foetal causes of IUGR?

A
  • Genetic abnormalities (trisomies 13/18/21, Turner’s)
  • Congenital infections (TORCH)
  • Multiple pregnancy
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168
Q

IUGR
What are some complications of IUGR?

A
  • Hypoglycaemia
  • Risk of necrotising enterocolitis
  • Neonatal jaundice
  • Hypothermia
  • Respiratory issues
  • Long-term sequelae include T2DM, HTN, obesity, behavioural problems, CP
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169
Q

IUGR
What causes…

i) hypoglycaemia?
ii) necrotising enterocolitis?
iii) neonatal jaundice?

A

i) Blood directed away from liver>brain so glycogen stores don’t develop adequately
ii) Reduced blood to bowel
iii) Compensatory polycythaemia for reduced oxygen supply from mother if reduced placental perfusion

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170
Q

IUGR
What causes…

i) hypothermia?
ii) respiratory problems?

A

i) No fat stores developed so cannot thermoregulate, large surface area
ii) Kidney hypoperfusion > decreased urine output > oligohydramnios > inadequate lung development

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171
Q

IUGR
What are the investigations for IUGR?

A
  • BP + urine dipstick (?pre-eclampsia)
  • Karyotyping (?foetal)
  • Infection screen, TORCH (?infection)
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172
Q

IUGR
When would you be concerned about IUGR?
What would you do?

A
  • SFH < 10th centile, slow or static growth or crossing centiles
  • Refer for serial growth scans (USS) every 2w, umbilical artery doppler + amniotic fluid volume
  • MCA doppler performed after 32w
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173
Q

IUGR
What is umbilical artery doppler for?
What happens if it’s abnormal?

A
  • Assesses if baby is getting enough blood
  • Abnormal = twice weekly review
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174
Q

IUGR
What is the management (and the indications of management) for IUGR?

A

Consider delivery (corticosteroids if <34w to mature foetal lungs) if –
- Static growth on growth charts
- Absent end-diastolic flow (AEDF, abnormal doppler)
- Abnormal CTG (foetal distress)
- MCA doppler PI <5% delivery by 37w (early sign of foetal hypoxia in SGA, shows increased diastolic flow > head-sparing effect)

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175
Q

MULTIPLE PREGNANCY
What is meant by a monozygotic multiple pregnancy?

A

identical (come from single zygote)

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176
Q

MULTIPLE PREGNANCY
What is meant by dizygotic multiple pregnancy?

A

non-identical (come from two different zygotes > diamniotic + dichorionic)

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177
Q

MULTIPLE PREGNANCY
What is meant by mono/diamniotic multiple pregnancy?

A

share/two separate amniotic sacs

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178
Q

MULTIPLE PREGNANCY
What is meant by a mono/dichorionic multiple pregnancy?

A

share/two separate placentas

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179
Q

MULTIPLE PREGNANCY
What are some predisposing factors to multiple pregnancies?

A
  • Previous twins,
    FHx,
    increasing parity + maternal age,
    IVF,
    race (Afro-Caribbean)
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180
Q

MULTIPLE PREGNANCY
What is one way of preventing them?

A

No more than 2 embryos transferred per IVF cycle

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181
Q

MULTIPLE PREGNANCY
What is the clinical presentation of multiple pregnancies?

A
  • Uterus larger than expected for dates
  • May suffer from hyperemesis gravidarum
  • Multiple foetal poles may be palpable at >24w
  • Multiple foetal hearts on auscultation
  • Majority diagnosed on dating scan
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182
Q

MULTIPLE PREGNANCY
What are some maternal and foetal complications of multiple pregnancy?

A
  • Anaemia, HTN, APH + PPH, preterm birth, stillbirth
  • Twin-twin transfusion syndrome, IUGR, polyhydramnios, malpresentation
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183
Q

MULTIPLE PREGNANCY
What is twin-twin transfusion syndrome?

A
  • Associated with monoamniotic monochorionic twins
  • Recipient gets majority of blood so is larger with polyhydramnios
  • Donor is starved of blood + can become anaemic, recipient worse off (hydrops)
  • Severe cases > laser ablation of connecting vessels
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184
Q

MULTIPLE PREGNANCY
What is the antenatal care for multiple pregnancies?

A
  • High risk –5mg folic acid, iron supplements to prevent anaemia
  • Additional scans for growth restriction + twin-twin transfusion (2w from 16w for monochorionic, 4w from 20w for dichorionic)
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185
Q

MULTIPLE PREGNANCY
What is the management of multiple pregnancies?

A
  • Steroids if <34w
  • Monochorionic/amniotic twins = elective c-section 32-34w
  • Diamniotic twins = 37–38w, vaginal if presenting twin cephalic but may need c-section for second
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186
Q

OLIGOHYDRAMNIOS
What is oligohydramnios?
What is it defined as?

A
  • Abnormally low levels of amniotic fluid during pregnancy
  • Amniotic fluid index <5th centile for gestational age
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187
Q

OLIGOHYDRAMNIOS
What are some causes of oligohydramnios?

A
  • PROM or SROM
  • Renal agenesis (Potter’s syndrome) or non-functional kidneys
  • Placental insufficiency (pre-eclampsia, post-term gestation) as blood redistributed to brain so reduced urine output
  • Genetic anomalies
  • Obstructive uropathy
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188
Q

OLIGOHYDRAMNIOS
What is the clinical presentation of oligohydramnios?

A
  • May have experienced leaking fluid or feeling damp
  • Measure SFH
  • Sterile speculum may show pool of liquor in birth canal
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189
Q

OLIGOHYDRAMNIOS
What are some investigations for oligohydramnios?

A
  • USS foetus = AFI or maximum pool depth calculated + doppler
  • TORCH screen as may be infection
  • Test fluid for IGFBP-1 or PAMG-1 if concerned about PPROM.
  • Foetal CTG for signs of distress
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190
Q

OLIGOHYDRAMNIOS
What are some complications of oligohydramnios?

A
  • 2nd trimester = poor prognosis due to PPROM leading to premature delivery + pulmonary hypoplasia > resp distress
  • Muscle contractures as amniotic fluid allows foetal to move limbs in utero
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191
Q

OLIGOHYDRAMNIOS
What is the management of oligohydramnios?

A
  • Treat as PROM if present
  • Frequent monitoring of growth for IUGR
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192
Q

POLYHYDRAMNIOS
What is amniotic fluid (liquor)?

A
  • Fluid between baby + amnion (sac) acts as a cushion around foetus to protect it from trauma
  • Foetus can swallow amniotic fluid which helps create urine + meconium
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193
Q

POLYHYDRAMNIOS
What is polyhydramnios?

A
  • Abnormally large levels of amniotic fluid
  • AFI >95th centile for gestational age
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194
Q

POLYHYDRAMNIOS
What are the causes of polyhydramnios?

A
  • Increased foetal urine production (maternal DM), twin-twin transfusion, foetal hydrops
  • Foetal inability to swallow/absorb amniotic fluid (GI tract obstruction e.g. duodenal atresia, foetal neuro/muscular issues)
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195
Q

POLYHYDRAMNIOS
How may polyhydramnios present?

A
  • Maternal discomfort
  • LGA
  • Foetal parts hard to palpate
  • Taut uterus
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196
Q

POLYHYDRAMNIOS
What are the investigations for polyhydramnios?

A
  • Exclude GDM with OGTT
  • USS foetus to calculate AFI or maximum pool depth
  • TORCH screen as can be cause by viral infections
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197
Q

POLYHYDRAMNIOS
What are some complications of polyhydramnios?

A
  • Preterm delivery
  • Malpresentation
  • Maternal discomfort from abdo distension
198
Q

POLYHYDRAMNIOS
What is the management of polyhydramnios?

A
  • If severe = amnioreduction or NSAIDs (indomethacin)
  • If preterm assess risk of delivery with cervical scan ± foetal fibronectin assay
199
Q

POLYHYDRAMNIOS
What are the risks of amnioreduction and indomethacin?

A
  • Associated with infection + placental abruption
  • Associated with premature closure of ductus arteriosus so not used beyond 32w
200
Q

RHESUS DISEASE
What are rhesus antigens?

A
  • On surface of red blood cells + differs to the ABO groups
  • A+ve is blood group A with rhesus D antigens
201
Q

RHESUS DISEASE
What is the pathophysiology of rhesus disease in the first pregnancy?

A
  • Rh-ve woman exposed to Rh+ve foetal blood, her immune system recognises as foreign + produce antibodies against rhesus D (sensitisation)
  • Usually no issues in 1st pregnancy as IgM produced that cannot cross placenta
202
Q

RHESUS DISEASE
What is the pathophysiology of rhesus disease in subsequent pregnancies?

A
  • Memory cells produce IgG which can cross placenta so if Rh+ve foetus will attack leading to haemolysis (haemolytic disease of newborn) with jaundice + hydrops fetalis (abnormal accumulation of fluid)
203
Q

RHESUS DISEASE
What events are considered potential sensitising events?

A
  • Delivery of Rh+ve infant
  • APH
  • Amniocentesis or CVS
  • Abdo trauma
  • ECV
  • Surgical Mx of ectopic + miscarriage
  • PV bleed >12w
204
Q

RHESUS DISEASE
What are some investigations for rhesus disease?

A
  • Kleihauer test (check how much foetal blood > mother’s blood after event)
  • All babies born to Rh-ve women should have cord blood at delivery for FBC, blood group + Direct Coombs (antiglobulin) test for antibodies on baby’s RBC
205
Q

RHESUS DISEASE
What is the Kleihauer test?

A
  • Add acid + foetal Hb more resistant to acid so number of cells that still contain Hb represents remaining foetal cells
206
Q

RHESUS DISEASE
What is the management of rhesus disease?

A
  • Prophylaxis crucial as sensitisation is irreversible
  • IM anti-D routinely at 28w, 34w + after birth but also potential events
  • Newborn haemolysis > exchange transfusions (severe) or UV phototherapy
207
Q

RHESUS DISEASE
How does anti-D work?

A
  • Immunoglobulin attaches to Rh D antigens on foetal blood in maternal circulation preventing recognition
208
Q

GESTATIONAL DIABETES
What is Gestational Diabetes Mellitus (GDM)?

A
  • Carbohydrate intolerance during pregnancy which often resolves after birth
209
Q

GESTATIONAL DIABETES
What is the pathophysiology of GDM?

A
  • Increased insulin resistance due to placental production of anti-insulin hormones
  • Allows post-prandial glucose peak to be higher for longer to spare glucose for foetus (main source of nutrients)
  • If maternal pancreas cannot increase insulin production to combat this > GDM
210
Q

GESTATIONAL DIABETES
What are some anti-insulin hormones produced by the placenta?

A
  • Main one is human placental lactogen (hPL)
  • Also glucagon + cortisol
211
Q

GESTATIONAL DIABETES
What are some risk factors for GDM?

A
  • BMI >30kg/m^2
  • PMH of GDM
  • FHx of DM (first-degree)
  • Asian + Afro-Caribbean ethnicity
  • Previous macrosomic baby
212
Q

GESTATIONAL DIABETES
What is the clinical presentation of GDM?

A
  • May be asymptomatic or present with polydipsia, polyuria, nocturia + fatigue
213
Q

GESTATIONAL DIABETES
What is the diagnostic investigation for GDM?
Who is given this?

A
  • OGTT (75g glucose given in morning after a fast)
  • Anyone with previous GDM at booking + 24–28w
  • Anyone with risk factors at 24-28w
214
Q

GESTATIONAL DIABETES
What OGTT results are diagnostic for GDM?

A

5-6-7-8 rule:
- Baseline/fasting >5.6mmol/L
- At 2h >7.8mmol/L

215
Q

GESTATIONAL DIABETES
What are the foetal risks of GDM?

A
  • Macrosomia
  • Polyhydramnios
  • Birth trauma
  • Stillbirth + miscarriage
  • Congenital malformations (CHD, NTD, cleft palate)
  • Neonatal hypoglycaemia
  • RDS, polycythaemia
  • Obesity + T2DM later in life
216
Q

GESTATIONAL DIABETES
What causes macrosomia?

A

Excess foetal glucose > hyperinsulinaemia + so increased fat deposition

217
Q

GESTATIONAL DIABETES
What causes polyhydramnios?

A

Excess foetal glucose > polyuria

218
Q

GESTATIONAL DIABETES
What causes birth trauma?

A

Cephalopelvic incompatibility, shoulder dystocia

219
Q

GESTATIONAL DIABETES
What causes neonatal hypoglycaemia?

A

Climatization + hyperinsulinaemia

220
Q

GESTATIONAL DIABETES
What are the maternal risks of GDM?

A
  • Pre-eclampsia
  • DKA or hypos
  • UTIs
  • IHD
  • Nephropathy, retinopathy
221
Q

GESTATIONAL DIABETES
What pre-conceptual advice should be given to women with pre-existing diabetes?

A
  • Contraception until good diabetic control
  • 5mg folic acid until 12w
  • Stop any ACEi or statins
  • Retinopathy screening at booking + 28w
  • Aspirin 75mg OD at 12w to reduce pre-eclampsia risk
  • Monitor BMs regularly
222
Q

GESTATIONAL DIABETES
What is the management of pre-existing T1DM?

A

Insulin with dose adjustment for normal changes to glucose metabolism in pregnancy

223
Q

GESTATIONAL DIABETES
What is the management of pre-existing T2DM?

A

Only metformin is safe, may need upgrading to insulin

224
Q

GESTATIONAL DIABETES
What is the management of GDM?

A
  • Fasting glucose <7 = lifestyle (low GI foods, exercise) > metformin after 1-2w if targets not met
  • Fasting glucose ≥7 = insulin ± metformin
  • Fasting glucose ≥6 + macrosomia or other complications = insulin
  • Glibenclamide if cannot tolerate metformin or decline insulin
225
Q

GESTATIONAL DIABETES
When should the foetus be delivered in…

i) pre-existing DM?
ii) GDM

A

i) 37–39w
ii) No need before 41w

226
Q

VTE IN PREGNANCY
What is VTE?
What is the significance?

A
  • DVTs + PEs = large cause of mortality in obstetrics
  • High risk during postpartum period, top cause of direct maternal death
227
Q

VTE IN PREGNANCY
What are the…

i) high
ii) intermediate

risk factors of VTE?

A

i) PMH of VTE, antenatal LMWH requirements, high-risk thrombophilia or low risk + FHx
ii) Smoking, parity >3, age >35, BMI >30, reduced mobility, multiple pregnancy, pre-eclampsia, gross varicose veins, IVF

228
Q

VTE IN PREGNANCY
What is the clinical presentation of VTE in pregnancy?

A
  • Swollen, warm, tender, red calf, Homan’s sign (calf pain on dorsiflexion) > DVT
  • SOB, sudden CP (pleuritic), haemoptysis, tachycardia > PE
229
Q

VTE IN PREGNANCY
What are the investigations for VTE?

A
  • ECG in PE commonly shows sinus tachycardia, rarely S1Q3T3
  • Doppler USS diagnostic for DVT
  • FBC, U+Es, LFTs, clotting screen, CXR if ?PE
  • CTPA gold standard for PE, can do V/Q scan
230
Q

VTE IN PREGNANCY
How do you manage VTE risk in pregnancy?

A
  • Risk assessment at booking, antenatal admissions + postnatally
  • Antenatal: LMWH from 28w if increased risk or ASAP if high risk
  • Postnatal: LMWH for 10d if increased risk or 6w if high risk
  • TED stockings
  • Low risk Mx = mobilise early, hydration
231
Q

VTE IN PREGNANCY
What is the management of a VTE event?
Any contraindications?

A
  • Embolectomy + anticoagulate ASAP with LMWH
  • Do NOT use warfarin (or DOACs) as can cross placenta + may cause foetal abnormalities (CHD) + intracranial bleeding
232
Q

OBSTETRIC CHOLESTASIS
What is obstetric cholestasis?

A
  • Intrahepatic cholestasis = reduced outflow of bile acids from liver
233
Q

OBSTETRIC CHOLESTASIS
What are some associations?

A
  • Asian women, thought to be due to increased oestrogen + progesterone levels
234
Q

OBSTETRIC CHOLESTASIS
What is the clinical presentation of obstetric cholestasis?

A
  • Typically later in pregnancy (3rd trimester)
  • Itchy skin (palms of hands + soles of feet) but with NO rash – WORSE at night
  • Jaundice, pale greasy stools + dark urine less common
235
Q

OBSTETRIC CHOLESTASIS
What are the investigations for obstetric cholestasis?

A
  • Clotting screen (prothrombin time) deranged
  • Abnormal LFTs + raised bile acids (ALT, AST, GGT + bilirubin raised, ALP too but that is normal in pregnancy), monitor LFTs weekly
236
Q

OBSTETRIC CHOLESTASIS
Why can clotting be deranged in obstetric cholestasis?

A
  • Bile acids important for fat soluble vitamin absorption like vitamin K
237
Q

OBSTETRIC CHOLESTASIS
What are the complications of obstetric cholestasis?

A
  • Maternal = vitamin K deficiency (may lead to PPH)
  • Foetal = stillbirth (#1), increased risk of prematurity (often iatrogenic)
238
Q

OBSTETRIC CHOLESTASIS
What is the management of obstetric cholestasis?

A
  • Ursodeoxycolic acid first line to improve LFTs + bile acids
  • Induce labour at 37–38w to reduce stillbirth risk
  • Vitamin K supplementation
  • Emollients (calamine lotion to sooth skin)
  • Antihistamines to help sleep
239
Q

INFECTIONS + PREGNANCY
What is Group B strep (GBS) infection?

A
  • Infection caused by Strep agalactiae
240
Q

INFECTIONS + PREGNANCY
What can Group B strep (GBS) infection in pregnancy cause?

A

Most common cause of early-onset severe infection (Sepsis) in neonates

241
Q

INFECTIONS + PREGNANCY
How is group B strep infection spread?

A

Commonly found in maternal bowel flora

242
Q

INFECTIONS + PREGNANCY
What are the risk factors of group B strep?

A
  • Prematurity,
  • prolonged ROM,
  • previous GBS sibling,
  • maternal pyrexia
243
Q

INFECTIONS + PREGNANCY
When should you screen?

A

If previous GBS in pregnancy either intrapartum IV Abx prophylaxis or test in late pregnancy (3-5w before EDD) + IV Abx if +ve

244
Q

INFECTIONS + PREGNANCY
When would you give intrapartum IV Abx?
What would you give?

A
  • Previous baby with GBS (no screening), preterm labour or pyrexia >38 during labour
  • Benzylpenicillin
245
Q

INFECTIONS + PREGNANCY
What are the risks of Varicella zoster?

A
  • Maternal risk = 5x greater risk of pneumonitis
  • Foetal varicella syndrome = skin scarring, microphthalmia, limb hypoplasia, microcephaly + learning difficulties
246
Q

INFECTIONS + PREGNANCY
What is the management of chickenpox exposure in pregnancy?

A
  • Any doubt in immunity, check for varicella zoster IgG
  • ≤20w + not immune = VZIG within 10d
  • > 20w + not immune = VZIG or aciclovir days 7–14 post-exposure
247
Q

INFECTIONS + PREGNANCY
What is the management of chickenpox infection in pregnancy?

A
  • PO aciclovir if ≥20w + presents within 24h of rash onset
  • <20w then consider
248
Q

ANAEMIA + PREGNANCY
Why is anaemia common in pregnancy?

A
  • Hb normally falls slightly in pregnancy due to increased plasma volume diluting Hb
249
Q

ANAEMIA + PREGNANCY
What are some causes?

A

Physiological,
Fe deficiency (increased demand),
B12 or folate deficiency

250
Q

ANAEMIA + PREGNANCY
What are some risk factors?

A

Menorrhagia,
malaria,
hookworm,
twins,
poor diet

251
Q

ANAEMIA + PREGNANCY
What are some investigations for anaemia?

A
  • FBC (normal ranges >110g/L at booking, >105g/L at 28w)
  • Microcytic hypochromic = Fe deficiency
  • Macrocytic = B12 or folate
  • Iron studies = TIBC (high), serum iron (low), serum ferritin (low but acute phase)
  • Haematinics, intrinsic factor Ab if ?pernicious
252
Q

ANAEMIA + PREGNANCY
What are the complications of iron deficiency anaemia?
How is it managed?

A
  • LBW + preterm delivery
  • Ferrous sulfate 200mg TDS
  • If not anaemic but low ferritin indicating iron stores then start them on it
  • Vitamin C can increase absorption of iron
253
Q

ANAEMIA + PREGNANCY
What is the management of macrocytic anaemias?

A
  • Pernicious = IM hydroxocobalamin
  • B12 deficiency = B12 tablets (cyanocobalamin)
  • Folate = increased from 400mcg to 5mg/day to reduce NTD.
254
Q

PROM
What is the physiology of ruptured membranes?

A
  • Foetal membranes = chorion + amnion strengthened by collagen
  • SROM occurs naturally at any point prior to or during labour due to weakening in chorion/amnion, rarely born en caul
  • ARM can augment or induce labour
255
Q

PROM
What is prelabour rupture of membranes?

What are the risks?

A

Rupture of amniotic sac at least 1h prior to onset of labour at >37w

  • minimal risk as advanced gestation
256
Q

PROM
What is

i) prelabour rupture of membranes?
ii) preterm prelabour rupture of membranes?

What are the risks?

A

i) Rupture of amniotic sac at least 1h prior to onset of labour at >37w
ii) Rupture of amniotic sac prior to onset of labour pre-term (<37w)
- PROM = minimal risk as advanced gestation
- PPROM = risk of chorioamnionitis + spontaneous labour

257
Q

PROM
What are some risk factors for (P)PROM?

A
  • Previous PROM/preterm
  • Smoking
  • Polyhydramnios
  • Amniocentesis
258
Q

PROM
What is the clinical presentation of (P)PROM?

A
  • Gush or constant trickle or dampness from vagina
  • Clear fluid
259
Q

PROM
What are some investigations for PROM?

A
  • Sterile speculum 1st for pooling of amniotic fluid
  • USS may show oligohydramnios if speculum normal
  • Ferning test (cervical secretion on glass slide shows fern-pattern crystals)
  • Test fluid for IGFBP-1 or PAMG-1
  • CTG for foetus (tachycardia is suggestive of infection)
260
Q

PROM
What is IGFBP-1 or PAMG-1?

A
  • Insulin-like growth factor-binding protein-1
  • Placental alpha-microglobin-1
  • High concentrations of these proteins in amniotic fluid
261
Q

PROM
What are some complications of PPROM?

A
  • Risk of prematurity, chorioamnionitis, pulmonary hypoplasia
262
Q

PROM
What is the management of PPROM?

A
  • 1st line = IM corticosteroids if foetus <34w
  • Prophylactic PO erythromycin given to prevent chorioamnionitis for 10d or until labour is established if within 10d
  • Consider induction at 34w (trade off)
263
Q

STAGES OF LABOUR
What is the WHO definition of normal birth?

A
  • Spontaneous in onset, low risk at start + remaining throughout labour + delivery
  • Infant born spontaneously in the vertex position between 37–42w
  • After birth, mother + infant are in good condition (aka no interventions)
264
Q

STAGES OF LABOUR
What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
265
Q

STAGES OF LABOUR
What is the role of prostaglandins in labour?

A

Aids with cervical ripening (effacement)

266
Q

STAGES OF LABOUR
What is the role of oxytocin in labour?

A

Produced by hypothalamus, secreted by post. pituitary, surge at labour inhibits progesterone to prepare smooth muscle for uterine contractions, milk ejection reflex postpartum

267
Q

STAGES OF LABOUR
What is the role of oestrogen in labour?

A

Surges at onset of labour to inhibit progesterone to prepare smooth muscle for labour

268
Q

STAGES OF LABOUR
What is the role of beta-endorphins in labour?

A

Natural pain relief

269
Q

STAGES OF LABOUR
What is the role of adrenaline in labour?

A

Released as birth imminent to give energy

270
Q

STAGES OF LABOUR
What is the role of prolactin in labour?

A

Produced + secreted by ant. pituitary, allows process of milk production in mammary glands when oestrogen + progesterone decline postpartum

271
Q

STAGES OF LABOUR
What is the role of relaxin in labour?

A

Released from placenta to soften ligaments + cartilage of pelvis so it can expand (cervix, vaginal tissues, perineum)

272
Q

STAGES OF LABOUR
What are Braxton-Hicks contractions?

A
  • ‘Practice’ contractions from 3rd trimester
  • Irregular + not felt by everyone
  • Mild cramp, last few minutes then ease
273
Q

STAGES OF LABOUR
What are signs of labour?

A
  • Show (shedding of mucus plug from cervix that prevents ascending bacteria)
  • Rupture of membranes
  • Shortening + dilation of cervix
  • Regular painful contractions
274
Q

STAGES OF LABOUR
What is the physiology of contractions?

A
  • Start in fundus (pacemaker)
  • Retraction/shortening of muscle fibres with each contraction pulls lower segment of uterus towards fundus
  • Causes cervical dilation + forces foetus down causing pressure on cervix
275
Q

STAGES OF LABOUR
What is the first stage of labour?
How is it further divided?

A
  • From onset of labour (true contractions) until the cervix is fully dilated
  • Latent phase = from 0–3cm dilation
  • Active phase = from 3–10cm
276
Q

STAGES OF LABOUR
What is the difference between latent and active phase of the first stage of labour?

A
  • Latent: cervix begins to efface, irregular contractions, ‘show’, can last 2–3d (usually 6h)
  • Active: stronger, more regular contractions (4:10), cervix continues effacing
277
Q

STAGES OF LABOUR
How quickly are women expected to dilate during the active phase?

A
  • Primis = 0.5cm/h,
  • multiparous = 1cm/h
278
Q

STAGES OF LABOUR
What is the second stage of labour?
How is it further divided?

A
  • From full dilation to delivery of the foetus
  • Passive stage: complete dilation but no pushing (often 1 hour)
  • Active stage: maternal pushing until delivery
279
Q

STAGES OF LABOUR
What is considered a delay in the active second stage of labour?
What does success depend on?

A
  • > 2h in nulliparous, 1h in multiparous
  • 3Ps (power, passenger + passage [?Psyche of mum])
280
Q

STAGES OF LABOUR
Once the foetus has been delivered, what should be assessed and when?
What does it calculate?

A
  • APGAR score
  • 1, 5 + 10 minutes
  • 10–7 = normal
  • 6–4 = moderately depressed
  • <4 = severely depressed
281
Q

STAGES OF LABOUR
What are the parts of the APGAR score?

A

Activity – absent 0, flexed arms + legs 1, active 2
Pulse – absent 0, <100bpm 1, >100bpm 2
Grimace – floppy 0, minimal response to stimulation 1, prompt response to stimulation 2
Appearance – blue 0, blue extremities 1, pink 2
Respiration – absent 0, slow + irregular 1, vigorous cry 2

282
Q

STAGES OF LABOUR
What is the third stage of labour?
What should it involves?

A
  • From birth of the foetus to expulsion of placenta
  • Physiological Mx = placenta delivered by maternal effort without medications or cord traction, cord clamped + cut after stops pulsating
283
Q

STAGES OF LABOUR
What should be done after delivery of the placenta?

A
  • Examine placenta + membranes to check complete as RPOC can cause serious PPH or infection
284
Q

STAGES OF LABOUR
What can be used when monitoring labour?

A

Partogram is graphic record of key maternal + foetal data –
- FHR every 15m (low risk = intermittent auscultation) high = continuous CTG
- Contractions every 30m (4 in 10 in established labour)
- Maternal pulse every 60m
- Maternal BP, temp, urine (ketones + protein) + VE to assess progress every 4h
- Drugs, IV fluids given + Cervical dilation noted too

285
Q

STAGES OF LABOUR
Why can partograms be useful?

A
  • Have alert + action line
  • Indicates slow progression so if at action line = take action
  • Provides clear guidance on when to intervene, alert means be wary
  • Point at which progression stops is useful to see where problem is
286
Q

STAGES OF LABOUR
What are the 6 cardinal movements of labour?

A
  • Engagement + descent
  • Flexion
  • Internal rotation
  • Extension (crowning)
  • Restitution/external rotation
  • Expulsion
287
Q

STAGES OF LABOUR
What is engagement?

A
  • Passage of presenting part into pelvic inlet
  • Entire head felt = 5/5ths palpable aka not engaged
  • Unable to feel head = 0/5ths palpable aka fully engaged
  • Foetus is engaged when >50% of presenting part descended into pelvis
288
Q

STAGES OF LABOUR
What is descent?
How can descent be described?
What is descent encouraged by?

A
  • Downward passage of presenting part through bony pelvis
  • Position of baby’s head (cm) in relation to mother’s ischial spines
  • Increased abdo muscle tone and increased frequency + strength of contractions
289
Q

STAGES OF LABOUR
How can descent of the baby be described?

A

In relation to ischial spines in cm –
- –5 = baby high up at around the pelvic inlet
- 0 = head at ischial spines (engaged)
- +5 = foetal head descended further out

290
Q

STAGES OF LABOUR
What position is the foetal head during engagement and descent?

A
  • Occiput transverse
291
Q

STAGES OF LABOUR
What is flexion?

A
  • Uterine contractions exert pressure down foetal spine towards occiput + cause neck flexion, allowing circumference of foetal head to reduce
292
Q

STAGES OF LABOUR
What is internal rotation?
Why does it occur?

A
  • Foetus passively internally rotates from OT to OA/OP to allow shoulders to negotiate pelvic inlet
  • Pelvic inlet widest diameter is transverse (side-side)
293
Q

STAGES OF LABOUR
What is extension?

A
  • Foetal occiput slips beneath suprapubic arch allowing head to extend + foetal head is born, usually facing maternal back (occiput anterior)
294
Q

STAGES OF LABOUR
What is restitution?

A
  • Shoulders only now negotiating pelvic outlet so head externally rotates to face mother’s L/R medial thigh so shoulders can pass
  • Pelvic outlet widest diameter is A-P (front-back)
295
Q

STAGES OF LABOUR
What is expulsion?
How may this be assisted?

A
  • Ultimately ends with delivery of foetus
  • Gentle downwards traction > deliver shoulder below suprapubic arch
  • Gentle upwards traction > deliver posterior shoulder (caution with excessive force as may cause brachial plexus damage)
296
Q

STAGES OF LABOUR
What is caput?
What is moulding?

A
  • Diffuse swelling of scalp caused by pressure of scalp against dilating cervix during labour
  • Caput may lead to moulding of the head (oblong not round shape) but this often disappears after a few days
297
Q

FAILURE TO PROGRESS
What are the 2 types of abnormal progression in labour?

A
  • Slow from beginning (primary dysfunctional labour) –may be insufficient uterine contractions
  • Sudden slowing of labour (secondary arrest) – may be cephalopelvic disproportion
298
Q

FAILURE TO PROGRESS
How can you assess a woman failing to progress?

A
  • Palpate abdomen for lie, head + contractions (may need USS)
  • CTG, colour of amniotic fluid, VE
299
Q

FAILURE TO PROGRESS
What factors may influence the mode of delivery of a baby in failure to progress?

A
  • Baby size + presentation
  • Well-being of baby + mother
  • How long labour has been going on for
  • Maternal exhaustion
  • Pelvic adequacy
300
Q

FAILURE TO PROGRESS
What may be calculated when considering inducing labour?
What does it calculate?

A
  • Bishop score = used to calculate how likely spontaneous labour is to occur
  • Score <5 = unripe cervix (less likely for induction success)
  • Score >9 = favourable cervix ready for labour or induction
301
Q

FAILURE TO PROGRESS
What are the components of the Bishop score?

A
  • Cervical dilation – <1cm (0), 1-2 (1), 3-4 (2), >5cm (3)
  • Cervical consistency – firm (0), intermediate (1), soft (2)
  • Cervical effacement –<30% (0), 40-50 (1), 60-70 (2), 80% (3)
  • Cervical position – posterior (0), intermediate (1), anterior (2)
  • Foetal station – –3 (0), -2 (1), -1/0 (2), ≥1 (3)
302
Q

FAILURE TO PROGRESS
What are some methods of inducing labour?

A
  • Membrane sweep
  • Prostaglandin E2 (PGE2) pessary or gel like dinoprostone
  • Cervical ripening balloon (gently inflates + dilates cervix)
  • Amniotomy if not ruptured already
  • Oxytocin analogue (syntocinon) infusion to cause uterine contractions
303
Q

FAILURE TO PROGRESS
What is the process of a membrane sweep?

A
  • Done before meds to try + encourage labour to start on its own (promotes positive feedback of stretch > oxytocin release)
304
Q

FAILURE TO PROGRESS
What is the process of PGE2?
What might it be used for?

A
  • Stimulates contraction of uterine muscles + ripens cervix
  • Improve Bishop score by cervical ripening so can induce
  • Uterine hyperstimulation (>5 in 10 for 20m or contraction >2m)
  • ?Remove PGE2, ?terbutaline tocolytic
305
Q

FAILURE TO PROGRESS
What is a risk of PGE2?
How to manage that risk?

A
  • Uterine hyperstimulation (>5 in 10 for 20m or contraction >2m)
  • ?Remove PGE2, ?terbutaline tocolytic
306
Q

FAILURE TO PROGRESS
What are some indications and contraindications for inducing labour?

A
  • PROM, IUGR, pre-eclampsia, obstetric cholestasis
  • Severe degree of placenta praevia, transverse foetal lie, severe cephalopelvic disproportion, low Bishop score
307
Q

OBSTRUCTED LABOUR
What is obstructed labour?

A

Obstructed labour is the failure of the fetus to descend through the birth canal, because there is an impossible barrier (obstruction) preventing its descent despite strong uterine contractions.
The obstruction usually occurs at the pelvic brim, but occasionally it may occur in the pelvic cavity or at the outlet of the pelvis. When labour is prolonged because of failure to progress, there is a high risk that the descent of the fetus will become obstructed.

308
Q

OBSTRUCTED LABOUR
What are the different types of causes of obstructed labour?

A
  • Power (most common)
  • Passage
  • Passenger
  • Psyche (maternal exhaustion in second stage)
309
Q

OBSTRUCTED LABOUR
How can ‘power’ cause obstructed labour?

A
  • Poor or uncoordinated uterine contractions
  • Either the uyerine contractions are not strong enough to efface and dilate the cervix in the first stage of labour or the muscular effort of the uterus is insufficient to push the baby down the birth canal during the second stage.
  • Common in primigravida women
  • May need instrumental delivery or syntocinon
310
Q

OBSTRUCTED LABOUR
How can ‘passage’ cause obstructed labour?

A
  • Labour may be prolonged if the mother’s pelvis is too small for the baby to pass through or the pelvis has an abnormal shape, or if there is a tumour or other physical obstruction in the pelvis.
  • Common in developing countries, risk of infection, fistulas
311
Q

OBSTRUCTED LABOUR
How can ‘passenger’ cause obstructed labour?

A

The fetus is the passenger travelling down the birth canal. Prolonged labour may occur if the fetal head is too large to pass through the mother’s pelvis, or the fetal presentation is abnormal. Includes hydrocephalus.

312
Q

OBSTRUCTED LABOUR
what are the clinical signs of an obstructed labour?

A
  • Mother anxious, weak, exhausted
  • Rupture of membranes
  • Tachy, low blood pressure, high RR…
  • Foul smelling meconium from vagina
  • Concentrated urine
  • Oedema (vulva/cervix)
  • Caput
  • Malpresentation and Malposition
  • Bandl’s Ring
313
Q

OBSTRUCTED LABOUR
what are the investigations for an obstructed labour?

A
  • Partograph – rate of cervical dilatation vs rate of foetal head descent. Compares it with
    normal
314
Q

OBSTRUCTED LABOUR
what is the management of an obstructed labour?

A
  • C section
  • Supportive treatment (IV, analgesia…)
315
Q

OBSTRUCTED LABOUR
what are the complications of an obstructed labour?

A
  • Fistula - Vagina and bladder/rectum/ureter/urethra
  • Still birth
  • PPH
  • Shock/sepsis
  • Paralytic ileus
316
Q

MALPRESENTATION
What is malpresentation?
What are the different types?

A
  • Presenting part of foetus is not the vertex of the foetal head
  • Shoulder = c-section
  • Breech (leg/bottom) = ECV or c-section
  • Brow = c-section
  • Face = c-section likely
317
Q

FAILURE TO PROGRESS
What is the difference between brow and face presentation?

A
  • Brow: head between full flexion + extension, associated with mentovertical diameter (chin to highest point of vertex)
  • Face: head hyperextended >120, associated with submentobregmatic diameter (junction of neck/lower jaw to anterior fontanelle)
318
Q

FAILURE TO PROGRESS
In terms of ‘passenger’ in failure to progress, what is important about position?

A
  • Refers to foetal head position on VE
  • Anterior/posterior fontanelles as landmarks, OA ideal
  • If OP at delivery means head is at posterior quadrant of pelvis requiring greater rotation which can prolong labour
319
Q

FAILURE TO PROGRESS
How would you manage failure to progress in the first stage of labour?

A
  • PGE2 if low bishop score as if not cannot induce
  • Oxytocin infusion ± amniotomy (if membranes not ruptured) > reassess in 2h
  • CTG with foetal blood sample if concerns, consider c-section if doesn’t help
320
Q

FAILURE TO PROGRESS
How would you manage failure to progress in the second stage of labour?

A
  • Allow to push for 2h if nulliparous or 1h if multiparous
  • No imminent delivery obstetric review for ?instrumental or c-section
321
Q

FAILURE TO PROGRESS
How would you manage failure to progress in the third stage of labour?
What are the indications for management?

A
  • IM oxytocin to cause uterus contraction to expel placenta
  • Cord clamp + careful cord traction to guide placenta out
  • Haemorrhage or >60m delay in physiological management (delay in active Mx is >30m)
322
Q

FAILURE TO PROGRESS
What are the consequences of failure to progress?

A
  • Foetal = distress, hypoxia (HIE, cerebral palsy), morbidity + mortality
  • Maternal = bleeding, tears, amniotic fluid embolism
323
Q

BREECH
What is breech presentation?
What are the risks?

A
  • When baby’s buttocks/legs lies over the maternal pelvis
  • Longitudinal lie but head at fundus
  • Risk of hypoxia + trauma
324
Q

BREECH
What are some causes/risk factors for breech presentation?

A
  • Idiopathic
  • Prematurity as baby may not have turned itself yet
  • Previous breech
  • Uterine abnormalities (bicornuate uterus), fibroids
  • Placenta praevia
  • Foetal abnormalities (CNS malformation
  • Multiple pregnancy
  • Poly/oligohydramnios
325
Q

BREECH
What are the 3 types of breech presentation?

A
  • Extended (Frank) = most common, hips flexed, both legs extended with feet by head, buttocks presenting
  • Flexed (Complete) = hips + knees flexed so buttocks + feet presenting (Cannonballing)
  • Footling = one leg flexed, one extended, foot hanging through cervix
326
Q

BREECH
Which breech is most associated with cord prolapse and why?

A
  • Footling
  • Nothing to act as plug over cervix if membranes ruptured
327
Q

BREECH
What are the investigations for breech?

A
  • Ideally antenatal Dx with USS, if <36w unimportant unless in labour
  • Abdo exam = longitudinal lie, head palpated at fundus, presenting part not head, foetal heart best heard high up uterus
328
Q

BREECH
What is the management of breech?

A
  • External cephalic version to move baby to correct position at 37w
  • C-section if ECV unsuccessful or contraindicated
329
Q

BREECH
What are some contraindications for ECV?

A
  • Absolute = pre-eclampsia, APH, oligohydramnios, foetal compromise
  • Relative = maternal HTN, foetal abnormality, 1 previous c-section
330
Q

FOETAL LIE
What is foetal lie?
What are the 4 types of lie?

A
  • Position of the foetus in relation to the mother’s body
  • Longitudinal, transverse, oblique, unstable
331
Q

FOETAL LIE
What is longitudinal lie?

A

Straight up + down

332
Q

FOETAL LIE
What is transverse lie?

A

Side-side, foetus perpendicular to long axis of uterus

333
Q

FOETAL LIE
What is oblique lie?

A

Angle

334
Q

FOETAL LIE
What is unstable lie?

A

Lie is actively changing (may be transverse, longitudinal, cephalic or breech)

335
Q

FOETAL LIE
What are some risk factors for foetal lie?

A
  • Multiparity (>P2) with lax uterus (common)
  • Polyhydramnios, prematurity
  • Uterine abnormalities, fibroids
  • Placenta praevia
  • Foetal abnormalities
336
Q

FOETAL LIE
What are some investigations for foetal lie?

A
  • Abdo exam = neither head nor buttocks presenting
  • Transverse = ovoid uterus wider at sides, lower pole empty, head in flank
  • USS can be used to confirm lie, often antenatally
337
Q

FOETAL LIE
What are some complications of abnormal lie?

A
  • May result in pre-term rupture of membranes
  • Membrane rupture risks cord prolapse (longitudinal lie prevents descent of cord) so transverse lie = highest risk of prolapse
338
Q

FOETAL LIE
What is the management for foetal lie?

A

Stable but transverse –
- ECV >36w even in early labour if membranes intact
- C-section if fails or pt choice
Unstable lie –
- Admit whilst unstable from 37w so c-section if labour starts

339
Q

FOETAL LIE
What are the contraindications to ECV for transverse lie?

A
  • Maternal rupture in last 7d
  • Multiple pregnancy (except for 2nd twin)
  • Major uterine abnormality
340
Q

CTG
What are the indications for a continuous cardiotocography (CTG)?

A
  • During labour for every woman
  • High risk pregnancies
  • Pyrexia (?chorioamnionitis)
  • Severe HTN ≥160/110
  • Oxytocin use
  • Fresh bleeding
341
Q

CTG
How do you interpret a CTG?

A

Dr C Bravado –
- Dr = define risk (high risk = continuous
- C = contractions (bottom trace shows frequency)
- Bra = baseline rate
- V = variability
- A = accelerations
- D = decelerations
- O = overall assessment

342
Q

CTG
What might different foetal baseline rates tell you?

A
  • > 160 may be maternal pyrexia, prematurity, chorioamnionitis
  • <110 may be maternal beta-blockers, increased foetal vagal tone
343
Q

CTG
What does reduced variability tell you?

A
  • Reduced variability may be hypoxia, lactic acidosis, prematurity
  • 40m reduced variability accepted as baby may be sleeping
344
Q

CTG
What are accelerations?
What do they show you?

A
  • Rise in baseline HR by 15 for ≥15s
  • Reassuring as baby moving
345
Q

CTG
What are decelerations?
What are the 3 types and their causes?

A
  • Fall in baseline HR by 15 for ≥15s
  • Early = peak of contraction corresponds with trough of depression (head compression from uterine contraction = normal)
  • Late = deceleration after contraction (hypoxia = placental insufficiency, asphyxia)
  • Variable = vary in shape + timing (cord compression)
346
Q

CTG
What are the features of a reassuring CTG for…

i) baseline?
ii) variability?
iii) accelerations?
iv) decelerations?

A

i) 110–160bpm
ii) >5bpm
iii) Present
iv) Early

347
Q

CTG
What are the features of a non-reassuring CTG for…

i) baseline?
ii) variability?
iii) decelerations?

A

i) 100–109bpm or 161–180bpm
ii) <5bpm for 40–90m
iii) Variable

348
Q

CTG
What are the features of an abnormal CTG for…

i) baseline?
ii) variability?
iii) decelerations?

A

i) <100bpm or >180bpm
ii) <5bpm for >90m
iii) Late

349
Q

CTG
What makes a CTG…

i) suspicious?
ii) pathological?

A

i) 1 non-reassuring
ii) ≥2 non-reassuring or 1 abnormal

350
Q

CTG
What are the pros of CTGs?

A
  • Allows long-term monitoring
  • Can pick up on foetal distress
  • Can be on constantly to identify any slight changes
351
Q

CTG
What are the cons of CTGs?

A
  • No improvement in perinatal outcomes in low-risk pregnancies
  • Foetal exposure to USS ionisation
  • Ambulatory monitoring may not be possible
  • Doesn’t give true beat to beat FHR monitoring or morphological Ax of heart
352
Q

FOETAL ECG
What is a foetal ECG?
What are the pros?
What are the cons?

A
  • Obtained via scalp
  • Gold standard for FHR, true beat to beat information
  • Invasive, associated with scalp injury + perinatal infection, only during labour when membranes ruptured + >2cm dilated
353
Q

FOETAL ECG
What is an alternative to scalp ECG?

A
  • Abdominal foetal ECG
  • Can be used ambulatory at home but only for high risk, morphological analysis possible + non-invasive
354
Q

CORD PROLAPSE
What is cord prolapse?
What is the danger?

A
  • Umbilical cord descends below the presenting part of the foetus after rupture of the membranes
  • Presenting part can compress cord or exposure of cord leads to vasospasm > significant risk of foetal morbidity + mortality from hypoxia
355
Q

CORD PROLAPSE
What are some risk factors for cord prolapse?

A
  • Prematurity
  • Polyhydramnios
  • Long umbilical cord
  • Malpresentation (Footling breech + transverse lie)
  • Multiparity + multiple pregnancy
  • Placenta praevia
356
Q

CORD PROLAPSE
What are the investigations for cord prolapse?

A
  • Foetal CTG distress (heart decelerations + bradycardia)
  • Dx via VE (cord at introitus), speculum confirms
357
Q

CORD PROLAPSE
What is the management of cord prolapse?

A
  • 999/emergency buzzer, neonatal team
  • Fill bladder with 500ml warmed saline via catheter (elevate presenting foetal part + lift off cord)
  • Left lateral position with head down or knee-chest position
  • Presenting part pushed back into uterus to prevent compression
  • Avoid handling cord > vasospasm
  • Tocolytics like terbutaline (SABA) to abolish contractions if delivery not imminently available
358
Q

SHOULDER DYSTOCIA
What is shoulder dystocia?

A
  • Failure of anterior shoulder to pass under symphysis pubis after delivery of foetal head
359
Q

SHOULDER DYSTOCIA
What are some risk factors for shoulder dystocia?

A
  • Macrosomia
  • Maternal DM
  • High maternal BMI
  • Cephalopelvic disproportion
  • Post-maturity
  • Previous shoulder dystocia
360
Q

SHOULDER DYSTOCIA
What is the clinical presentation of shoulder dystocia?

A
  • Head remaining tightly applied to vulva or retracting (turtle neck sign)
  • Failure of restitution (head does not turn sideways)
361
Q

SHOULDER DYSTOCIA
What are the maternal and neonatal complications of shoulder dystocia?

A
  • PPH, perineal tears (3rd/4th degree), psychological impact
  • Hypoxia, cerebral palsy, injury to brachial plexus, Erb’s palsy, fits, # humerus or clavicle
362
Q

SHOULDER DYSTOCIA
Explain what is the result of…

i) erb’s palsy?
ii) clavicle fracture?

A

i) Injury of C5/6 nerves causing paralysis of arm, looks limp, waiters tip position
ii) Painful movements, shoulder asymmetry

363
Q

SHOULDER DYSTOCIA
What is the management of shoulder dystocia?

A

HELPERR[R] –
- Help (call with emergency buzzer, obs, neonates)
- Evaluate for episiotomy (enlarge opening)
- Legs = McRobert’s
- Pressure = suprapubic
- Enter = pelvis for rotation
- Remove = posterior arm
- Replace = head in vagina + deliver by section (Zavanelli)

364
Q

SHOULDER DYSTOCIA
What is McRobert’s manoeuvre?
Why is it done?

A
  • Hips fully flexed + abducted (knees to abdo)
  • Posterior pelvic tilt lifting symphysis pubis up + out of way
365
Q

SHOULDER DYSTOCIA
What are the 3 rotational manoeuvres?

A
  • Rubin II = pressure on post. aspect of ant. shoulder to help deliver under symphysis pubis
  • Woods’ screw = Rubin II + pressure on ant. aspect of post. shoulder
  • Reverse woods’ screw = pressure on ant. aspect of ant. shoulder + post. aspect of post. shoulder in opposite way
366
Q

INSTRUMENTAL DELIVERY
What are some indications for instrumental delivery?

A
  • Failure to progress in second stage.
  • Foetal or maternal distress + maternal exhaustion in second stage
  • Control of head in various foetal positions (incl. breech)
367
Q

INSTRUMENTAL DELIVERY
What are the types of instrumental delivery?

A
  • Ventouse = suction cup on a cord on baby’s head with traction
  • Forceps = 2 curved pieces of metal attach either side of baby’s head + grip with traction
368
Q

INSTRUMENTAL DELIVERY
What are the main risks of ventouse delivery?

A
  • Cephalohaematoma = collection of blood between periosteum + skull from damaged blood vessels, does not cross suture lines, presents hours after
  • Caput Succedaneum = Crosses Sutures, diffuse oedema outside periosteum due to pressure to a specific area of scalp, resolve in few days, conehead present at birth
369
Q

INSTRUMENTAL DELIVERY
What are the main risks of forceps delivery?

A
  • Maternal = vaginal tears, anal sphincter trauma
  • Foetal = facial nerve palsy (main), bruises on baby’s face, fat necrosis > hardened lumps of fat on baby’s cheek that will resolve spontaneously over time, skull #
370
Q

INSTRUMENTAL DELIVERY
What are some maternal consequences of instrumental delivery?

A
  • Infection (co-amox stat)
  • PPH
  • Episiotomy
  • Tears
  • Incontinence
371
Q

C-SECTION
What are some indications for c-section?

A
  • Placenta praevia (3/4)
  • IUGR
  • Uncontrolled HIV
  • Active herpes
  • Cephalopelvic disproportion
  • Pre-eclampsia
  • Post-maturity
372
Q

C-SECTION
What are the different categories of c-section?

A
  • 1 = immediate threat to life of mother/baby. Decision>delivery time = 30m
  • 2 = not imminent threat to life but c-section required urgently due to compromise. Decision>Delivery time = 75m
  • 3 = c-section required but both stable
  • 4 = elective section
373
Q

C-SECTION
What two types of anaesthesia can be used in c-sections?
What else is given in c-sections?

A
  • General
  • Regional block (spinal)
  • H2 receptor antagonists or PPIs, prophylactic Abx, oxytocin (PPH), LMWH for VTE prophylaxis
374
Q

C-SECTION
What are the indications for general anaesthesia?
What are the cons?

A
  • Imminent threat to mother ± foetus, C/I to regional, maternal preference, failed regional technique
  • Aspiration, failed intubation, awareness, damage to mouth/throat
375
Q

C-SECTION
What are the pros and cons for spinal anaesthesia?

A
  • Safer, see baby immediately, partner present, improved post-op analgesia
  • Hypotension, headache, discomfort with pressure sensations, failure
376
Q

C-SECTION
What are the complications of c-sections?

A
  • Surgical risk (bleeding, infection/endometritis, VTE)
  • Damage risk (ureter, bladder, bowel, vessels)
  • Future pregnancies (increased risk of uterine rupture, placenta praevia, stillbirth + repeat section)
  • Baby (risk of lacerations, increased incidence in transient tachypnoea)
377
Q

C-SECTION
Is vaginal birth after caesarean (VBAC) allowed?
What are the contraindciations?

A
  • Yes provided cause of caesarean is unlikely to recur, 75% success rate
  • Previous uterine rupture, classical caesarean scar
378
Q

PAIN RELIEF
What are some non-pharmacological pain relief for labour?

A
  • Trained support
  • Relaxation techniques, hypnotherapy
  • Massage, water births
  • Comfortable position + environment for birth
379
Q

PAIN RELIEF
What simple analgesia can be used in labour?

A
  • Paracetamol + codeine useful in early labour
  • Avoid NSAIDs
380
Q

PAIN RELIEF
What is Entonox?
What are the pros?
What are the cons?

A
  • Gas + air (N2O + O2 50/50 mixed)
  • Rapid onset analgesia, minimal SEs, self-limiting, available for home delivery
  • Theoretic risk of bone marrow suppression, greenhouse gas, N+V
381
Q

PAIN RELIEF
What opioids can be used for pain relief?

A
  • Single shot IM opioids (diamorphine, pethidine)
  • Patient-controlled analgesia via IV cannula (fentanyl, alfentanil, remifentanil)
382
Q

PAIN RELIEF
What are some important notes about single shot opioids?

A
  • Lipid soluble so crosses placenta rapidly
  • Diamorphine 2x as potent as morphine so faster onset
  • Pethidine metabolites can cause seizures so avoid in epileptics
383
Q

PAIN RELIEF
What are some important notes about PCA?

A
  • Fentanyl = very lipid soluble, rapid onset of action, long half-life
  • Alfentanil + remifentanil = shorter half-lives
384
Q

PAIN RELIEF
What are some side effects from opioids?

A
  • Foetal = resp depression, diminishes breast seeking + feeding behaviour
  • Maternal = euphoria + dysphoria, N+V, can prolong 1st + 2nd stages, resp depression + pruritus
385
Q

PAIN RELIEF
What regional techniques can be used for pain relief?
How is this performed?

A
  • Epidural, spinal or combined spinal epidural (CSE)
  • Epidural at L3/4 ‘Tuffiers’ line connecting 2 iliac crests bisects L4 vertebral body or USS to avoid cord damage
386
Q

PAIN RELIEF
What causes labour pain in…

i) first stage?
ii) second stage?

A

i) Uterine contraction at T10-L1
ii) Perineum + vaginal stretching S2-4 (pudendal)

387
Q

PAIN RELIEF
What 4 regimes can be given for regional techniques?

A
  • Intermittent = high conc LA, labour intensive, periods of inadequate analgesia + haemodynamic instability
  • Continuous = low dose LA + opioid, less labour intensive, constant analgesia + haemodynamic stability
  • Continuous + bolus = greater maternal satisfaction
  • CSE = rapid onset, high satisfaction, reduced LA dose
388
Q

PAIN RELIEF
What medications can be given epidurally?

A
  • LA like bupivacaine
  • Opioids like fentanyl, diamoprhine
389
Q

PAIN RELIEF
What sequential effects do regional techniques have?

A
  • Autonomic (vasodilation = reduced MAP)
  • Sensory (analgesia)
  • Motor (motor blockade) + fever
390
Q

PAIN RELIEF
What are the indications for regional techniques?

A
  • Maternal request
  • HTN/pre-eclampsia
  • Cardiac disease
  • Induced labour
  • Multiple births
  • Instrumental/op delivery likely
391
Q

PAIN RELIEF
What are some complications of regional techniques?

A
  • Potential for spinal cord damage
  • Hypotension + bradycardia
  • Haematoma/abscess at injection site
  • Anaphylaxis if allergic
  • Post-dural puncture headache
392
Q

PAIN RELIEF
What is a post-dural puncture headache?
How does it present?
What is the management?

A
  • Leak of CSF + reduced CSF pressure, within 1–2d (up to 7)
  • Headache, worse when upright, improves when flat
  • Supportive, pain >72h = epidural blood patch, IV caffeine
393
Q

PAIN RELIEF
What are some contraindications to regional techniques?

A
  • Absolute = maternal refusal, local infection, allergy to LA
  • Relative = coagulopathy, systemic infection, fixed cardiac output
394
Q

PAIN RELIEF
What are some side effects from regional techniques?

A
  • Foetal = tachycardia (maternal pyrexia), diminishes breast-feeding behaviour
  • Maternal = increased length of 1st + 2nd stages, need more oxytocin, increased need for instrumental, loss of mobility + bladder control, pyrexia
395
Q

PERINEAL TEARS
What is a perineal tear?

A
  • External vaginal opening is too narrow to accommodate the baby, leading to a ripping of the skin in that area as the baby’s head comes through
396
Q

PERINEAL TEARS
What is the classification of perineal tears?

A
  • 1st degree = limited to superficial skin of perineum
  • 2nd degree = above PLUS perineal muscles (includes episiotomy)
  • 3rd degree = above PLUS anal sphincter involvement
  • 4th degree = above PLUS injury to rectal mucosa
397
Q

PERINEAL TEARS
How are third degree tears further classified?

A
  • 3A = <50% of external anal sphincter thickness torn
  • 3B = >50% of EAS thickness torn
  • 3C = EAS + internal anal sphincter torn
398
Q

PERINEAL TEARS
What are some risk factors for perineal tears?

A
  • Primigravida
  • Macrosomia
  • Shoulder dystocia
  • Forceps
399
Q

PERINEAL TEARS
What is an episiotomy?

A
  • Diagonal incision (45 degrees) from opening of vagina downwards + laterally (medio-laterally) to avoid anal sphincter damage or midline in anticipation of needing additional room to delivery baby (e.g. prior to forceps) – suture after
  • Should be done under LA
400
Q

UTERINE RUPTURE
What is a uterine rupture?

A
  • Complication of labour where myometrium bursts
401
Q

UTERINE RUPTURE
What are the two types?

A
  • Incomplete = peritoneal lining surrounding uterus intact
  • Complete = peritoneal lining ruptures so uterine contents released into peritoneal cavity
402
Q

UTERINE RUPTURE
What is the risk?

A

Significant haemorrhage, high morbidity + mortality for baby + mother

403
Q

UTERINE RUPTURE
What are some risk factors for uterine rupture?

A
  • VBAC
  • Previous uterine surgery
  • Increased BMI
  • High parity
  • Congenital uterine abnormalities
  • Oxytocin use
404
Q

UTERINE RUPTURE
What are the clinical features of uterine rupture?

A
  • Tenderness over previous uterine scars
  • PV bleed, maternal shock
  • CTG = foetal distress + no or cessation of contractions
405
Q

UTERINE RUPTURE
What is the management of uterine rupture?

A
  • ABCDE resus
  • Cross match blood
  • Urgent laparotomy to stop bleeding
  • Repair or remove uterus
  • C-section to save baby
406
Q

PPH
What is a primary postpartum haemorrhage (PPH)?

A

Primary = loss of >500ml blood in the first 24h after delivery
- Minor = 500–1000ml estimated blood loss
- Major = >1000ml, clinically in shock

407
Q

PPH
What is a secondary postpartum haemorrhage (PPH)?

A

Secondary = excessive blood loss from genital tract between 24h–12w after delivery (can result in Sheehan’s syndrome)

408
Q

PPH
What are the primary causes of PPH?

A

Primary (4Ts)–
- Tone (uterine atony = most common)
- Trauma (perineal tear)
- Tissue (retained products)
- Thrombin (clotting issue e.g. DIC in pre-eclampsia)

409
Q

PPH
What are the secondary causes of PPH?

A

Secondary most common cause is retained placental tissue, endometritis

410
Q

PPH
What are the risk factors for PPH?

A
  • Before birth = previous PPH, APH, twins/triplets, pre-eclampsia, obesity, polyhydramnios
  • Labour = prolonged, c-section, perineal tear or episiotomy, macrosomia
411
Q

PPH
How might uterine atony present in PPH?

A
  • Unpalpable uterus on abdo exam (should normally be palpable in period following birth)
412
Q

PPH
What are some preventative measures to reduce risk and consequences of PPH?

A
  • Treat anaemia during antenatal period
  • Empty bladder (?catheter) as full bladder reduces uterine contractions
  • Active Mx of third stage (IM oxytocin)
  • IV TXA during c-section in third stage of labour if high risk
413
Q

PPH
What is the acute management of PPH?

A
  • ABCDE resus
  • 2x large bore cannulas
  • Group + X match
  • Activate major haemorrhage protocol for quick blood access
  • IV fluids/bloods
414
Q

PPH
What mechanical treatment can be trialled in PPH?

A
  • Rub uterus through abdomen to stimulate contraction
415
Q

PPH
What is the role of medical management in PPH?
What is the medical management of PPH?

A
  • All stimulate uterine contractions
  • IV syntocinon
  • IV/IM ergometrine, C/I in HTN as vasoconstrictor (can combine with syntocinon as syntometrine)
  • IM carboprost, caution in asthma (prostaglandin analogue)
  • Sublingual misoprostol (prostaglandin analogue)
416
Q

PPH
After failed medical management, what is the surgical management of PPH?

A
  • Intrauterine balloon tamponade (1st line in uterine atony)
  • B-lynch sutures (suture around uterus to compress it)
  • Internal iliac/uterine artery ligation (reduces blood flow to stop bleeding)
  • Hysterectomy as last resort (may save life)
417
Q

MENTAL HEALTH
What are some red flags in terms of maternal mental health?

A
  • Recent change in mental state or new Sx
  • New thoughts or acts of violence/self-harm
  • New + persistent feelings of incompetency as mother or estrangement from baby
418
Q

MENTAL HEALTH
Why can mental health disorders be difficult to detect in the puerperium?

A
  • Fear of treatment
  • Fear of children being removed
  • Cultural lack of recognition
  • Denial
  • Stigma
419
Q

BABY BLUES
What are baby blues?

A
  • Brief period of tearfulness, anxiety + emotional lability starting 3–10d after birth
420
Q

BABY BLUES
How common is it?

A

Affects up to 70% of women, classically primiparous

421
Q

BABY BLUES
What is the management?

A

Reassure natural to feel emotional + overwhelmed, health visitor obs

422
Q

POSTNATAL DEPRESSION
What is postnatal depression?

A
  • Depressive episode, temporally related to childbirth, within 6m post-partum
423
Q

POSTNATAL DEPRESSION
What are some risk factors?

A

PMH/FHx of MH issues,
Hx of abuse,
lack of support/relationships,
low socioeconomic status,
unemployed

424
Q

POSTNATAL DEPRESSION
What can be used to measure postnatal depression?

A
  • Edinburgh postnatal depression scale = screening tool, >10 suspect
425
Q

POSTNATAL DEPRESSION
How does postnatal depression present?

A

Typical depression
Sx but may include worries about baby’s health or ability to cope adequately, feeling detached from the baby

426
Q

POSTNATAL DEPRESSION
What is the management of postnatal depression?

A
  • Early identification + close monitoring of those at risk
  • CBT may help, sertraline + paroxetine if severe as safer in breastfeeding
  • ?Hospital admission if thoughts of self or baby-harm
427
Q

POSTPARTUM/PUERPERAL PSYCHOSIS
What is postpartum/puerperal psychosis?

A
  • Acute psychotic episode with peak occurrence at 2w postpartum
428
Q

POSTPARTUM/PUERPERAL PSYCHOSIS
What are some risk factors?

A

FHx/PMH of MH (esp. postpartum psychosis),
traumatic birth or pregnancy,
primiparous

429
Q

POSTPARTUM/PUERPERAL PSYCHOSIS
What is the clinical presentation of postpartum psychosis?

A
  • Prominent affective Sx (mania or depression with psychotic Sx)
  • Schizophreniform disorder (lasts <6m)
  • Emotional lability, delusions, hallucinations, suicidality, infanticide
430
Q

POSTPARTUM/PUERPERAL PSYCHOSIS
What is the management of postpartum psychosis?

A
  • Assess suicide risk + risk to baby
  • Often inpatient admission (mother + baby unit)
  • Antipsychotics ± antidepressants or mood stabilisers (carbamazepine), ECT for major affective disorder
  • Psychoeducation for pt + family, CBT
  • Children + family social service involvement
431
Q

OBESITY IN PREGNANCY
what are the risks for the mother relating to obesity in pregnancy?

A

o Maternal death or severe morbidity.
o Cardiac disease.
o Spontaneous 1st trimester or recurrent miscarriage.
o Pre-eclampsia.
o Gestational diabetes.
o Thromboembolism.
o Post-CS wound infection.
o Infection from other causes.
o PPH.
o Low breast-feeding rates.

432
Q

OBESITY IN PREGNANCY
what are the risks for the baby relating to obesity in pregnancy?

A

o Stillbirth and neonatal death.
o Congenital abnormalities.
o Prematurity

433
Q

CERVICAL SHOW
what is cervical show?

A
  • when the cervix effaces, the mucous plug comes loos and passes out of the vagina (could have blood)
  • seen in the latent phase.
434
Q

SICKLE CELL DISEASE IN PREGNANCY
what are the risks of sickle cell disease during pregnancy?

A
  • Crises are more common during pregnancy
  • Increased risk of pre-eclampsia
  • Increased risk of delivery by CS due to fetal distress
435
Q

SICKLE CELL DISEASE IN PREGNANCY
what are the foetal risks in sickle cell disease?

A
  • miscarriage
  • IUGR
  • prematurity
  • stillbirth
436
Q

SICKLE CELL DISEASE IN PREGNANCY
what is the management?

A
  • Pre-Pregnancy counselling
  • Stop iron chelating agents before pregnancy
  • Give folic acid and penicillin prophylaxis for hypersplenism
  • Screen for UTI infections each visit
  • Crisis Treatment: Analgesics, oxygen, hydration, and
    antibiotics if infection is suspected
  • Regular foetal monitoring
  • Aim for vaginal delivery
437
Q

FOETAL HYDROPS
what is foetal hydrops?

A

Fetal hydrops is the abnormal accumulation of serous fl uid in two or more fetal compartments. This may be pleural or pericardial effusions, ascites, skin oedema, polyhydramnios, or placental oedema.

438
Q

FOETAL HYDROPS
what are the different types?

A

immune and non-immune

439
Q

FOETAL HYDROPS
what is the pathophysiology?

A

an imbalance of interstitial fluid production and inadequate lymphatic return. This can result from congestive heart failure, obstructed lymphatic flow, or decreased plasma osmotic pressure.

440
Q

FOETAL HYDROPS
what are the causes of immune foetal hydrops?

A

results from blood group incompatibility between the mother and the fetus causing fetal anaemia.
THIS IS RHESUS DISEASE OF THE NEWBORN**

441
Q

FOETAL HYDROPS
what are the causes of non-immune foetal hydrops

A
  • severe anaemia (parvovirus B19, thalassaemia, G6PD)
  • cardiac abnormalities
  • chromosomal abnormalities (trisomies 13, 18 and 21)
  • genetic conditions
  • other infections (toxoplasmosis, rubella, CMV, varicella)
  • structural abnormalities (CCAM, diaphragmatic hernia)
  • twin-to-twin transfusion syndrome
  • chorioangioma
442
Q

FOETAL HYDROPS
what are the investigations?

A
  • ultrasound (diagnostic)
  • foetal blood/amniotic fluid sampling
  • maternal blood sampling
443
Q

FOETAL HYDROPS
what is the management?

A

depends on the cause
- anaemia = in-utero blood transfusion
- pleural effusions/CCAM = shunt
- twin-to-twin transfusion syndrome = laser photocoagulation of placental anastomoses
- cardiac arrhythmias = maternal digoxin + flecanide

444
Q

LOW BIRTH WEIGHT
what is a low birth weight defined as?

A

an infant born weighing 5.5 pounds (2500 grams) or less.
➢ Very low: less than 3.3 pounds
➢ Normal: 5.5 to 8.8 pounds
➢ High: more than 8.8 (could be due to GDM)

445
Q

LOW BIRTH WEIGHT
what are the risk factors for low birth weight?

A

➢ Low socioeconomic
➢ History of abuse
➢ Age (<15 or >35)
➢ Race (black, ethnic minorities…)

446
Q

LOW BIRTH WEIGHT
what are the causes of low birth weight?

A

➢ Preterm birth (before 37 weeks gestation)
➢ Genetics (could be chromosomal abnormalities…)
➢ Uteroplacental insufficiency
➢ Multiple pregnancy
➢ Substance abuse (smoking, drinking alcohol, illicit drug) causing IUGR
➢ Chronic conditions and infections (hypertension, rubella, CMV, syphilis, toxoplasmosis, BV…)
➢ Medications (sodium valproate, ramipril, warfarin…)

447
Q

LOW BIRTH WEIGHT
what are the consequences of a low birth weight?

A

➢ Feeding struggles
➢ Respiratory distress syndrome
➢ Jaundice
➢ Infections
➢ PDA
➢ Intraventricular hemorrhage
➢ Retinopathy of prematurity, and hearing problems
➢ Intellectual and developmental disabilities
➢ Diabetes
➢ High blood pressure
➢ Heart disease
➢ Obesity

448
Q

LOW BIRTH WEIGHT
what is the management?

A

➢ IV fluids or gavage feeding
➢ Light therapy
➢ Supplemental surfactant or oxygen
➢ Surgery or medications (ROP or PDA), and for intraventricular hemorrhage
➢ Kangaroo care (skin to skin contact)
➢ Primary prevention: Avoid drinking, smoking and unhealthy diet during pregnancy. Get the flu vaccine

449
Q

LOW BIRTH WEIGHT
what is the primary prevention for low birth weight?

A

Primary prevention: Avoid drinking, smoking and unhealthy diet during pregnancy. Get the flu vaccine

450
Q

UTEROPLACENTAL INSUFFICIENCY
what is it?

A

It is an uncommon but serious complication of pregnancy. It occurs when the placenta does not develop properly or is damaged. This blood flow disorder is marked by a
reduction in the mother’s blood supply. The complication can also occur when the mother’s blood supply doesn’t adequately increase by mid-pregnancy.

451
Q

UTEROPLACENTAL INSUFFICIENCY
what are the causes of uteroplacental insufficiency?

A

➢Abnormal trophoblast invasion:
▪ Pre-eclampsia
▪ Placenta accreta
➢ Abruption
➢ Infarction
➢ Placenta previa
➢ Tumor: chorioangiomas
➢ Abnormal umbilical cord or cord insertion (i.e., two vessel cord)
➢ Maternal diabetes
➢ Maternal hypertension
➢ Anemia
➢ Smoking
➢ Drug abuse (cocaine, heroin, methamphetamine)
➢ Antiphospholipid syndrome
➢ Renal disease
➢ Advanced age

452
Q

UTEROPLACENTAL INSUFFICIENCY
what is the presentation?

A

➢ Depending on the cause
➢ Mother may notice uterus is smaller than previous pregnancies
➢ Fetus may be moving less than expected
➢ IUGR
➢ Vaginal bleeding or preterm labor contractions (i.e., during placental abruption)

453
Q

UTEROPLACENTAL INSUFFICIENCY
what are the maternal complications?

A

preeclampsia,
placental abruption,
preterm labor, and delivery

454
Q

UTEROPLACENTAL INSUFFICIENCY
what are the foetal complications?

A

Oxygen deprivation (cerebral palsy),
learning disabilities,
hypothermia,
hypoglycemia,
hypocalcemia,
polycythemia,
premature labor,
stillbirth,
death

455
Q

UTEROPLACENTAL INSUFFICIENCY
what are the investigations?

A

➢ USS
➢ Maternal alpha fetoprotein levels
➢ CTG

456
Q

UTEROPLACENTAL INSUFFICIENCY
what is the management?

A

➢ Avoid precipitating factors (drugs, smoking, alcohol…
➢ Treat underlying cause
➢ Education on preeclampsia, frequent monitoring, possibly steroid injections, possible delivery.
➢ FETAL SURVEILLANCE

457
Q

PUERPERAL INFECTION
what is it defined as?

A

Temperature of above 38 degrees Celsius in the first 14 days following delivery.

458
Q

PUERPERAL INFECTION
what are the genital causes?

A
  • uterine infection
  • perineal wound infection
459
Q

PUERPERAL INFECTION
what are the predisposing factors for uterine infection?

A
  • Caesarean section,
  • Pre-labour rupture of membranes,
  • Intrapartum chorioamnionitis,
  • Prolonged labor,
  • Multiple pelvic examinations,
  • Internal fetal monitoring—use of scalp electrodes/intrauterine pressure catheters,
  • other risk factors, e.g., anemia, low socio-economic status.
460
Q

PUERPERAL INFECTION
what is the presentation of uterine infection?

A

Fever usually in proportion to the extent of infection.
Foul smelling, profuse, and bloody discharge.
Subinvolution of uterus.
Tender bulky uterus on abdominal examination.

461
Q

PUERPERAL INFECTION
what are the non-genital causes?

A
  1. Breast causes (mastitis, abscess)
  2. UTI (i.e., from catheter, hypotonic bladder, KEEPS bacteria)
  3. Thrombophlebitis (high risk of DVT and PE)
  4. Respiratory complications (mainly women with CS; due to atelectasis, aspiration, or bacterial pneumonia) – hence the need for prophylactic antibiotics before CS!
  5. Abdominal wound infection
462
Q

PUERPERAL INFECTION
what are the investigations?

A

➢ FBC
➢ Blood Cultures
➢ MSU
➢ Swabs from cervix and lochia for chlamydia and bacterial infections
➢ Wound swabs
➢ Throat swabs
➢ Sputum culture and CXR

463
Q

PUERPERAL INFECTION
what is the management?

A

➢ Supportive (analgesics/NSAIDS, wound care, ice packs…)
➢ Antibiotics (for endometritis – IV clindamycin and gentamicin until >24hrs afebrile)
➢ Surgical (drain abscess, secondary repair of wound, drainage of hematomas…)

464
Q

CHLAMYDIA IN PREGNANCY
what are the risks of chlamydia infection during pregnancy?

A
  • preterm labour
  • PROM
  • low birth weight
  • infection during delivery (conjunctivitis and pneumonia)
465
Q

CHLAMYDIA IN PREGNANCY
what is the management?

A
  • azithromycin 1g OD followed by 500mg orally OD for 2 days
  • erythromycin 500mg QD for 7 days
  • amoxicillin 500mg TD for 7 days
466
Q

GONORRHOEA IN PREGNANCY
what are the risks?

A
  • miscarriage
  • premature birth
  • low birth weight
  • PROM
  • chorioamnionitis
  • eye infection in newborn
467
Q

GONORRHOEA IN PREGNANCY?
what is the management?

A

500mg ceftriaxone IM single dose

468
Q

SYPHILIS IN PREGNANCY
what are the risks?

A

congenital syphilis
- premature births
- still births
- multi-organ problems to brain, eyes, heart, skin, teeth and bones

469
Q

SYPHILIS IN PREGNANCY
what is the management?

A

penicillin

470
Q

TRICH VAGINALIS IN PREGNANCY
what are the risks?

A
  • PROM
  • preterm births
  • low birth weight
  • female newborns can acquire infection during birth
471
Q

TRICH VAGINALIS IN PREGNANCY
what is the management?

A

metronidazole

472
Q

UTIs IN PREGNANCY
why are UTIs more common in pregnancy?

A

due to dilation of the upper renal tract and urinary stasis (hypoactive bladder)

473
Q

UTIs IN PREGNANCY
why are pregnant women screened for asymptomatic bacteriuria at their booking visit?

A

it can lead to symptomatic infection if left untreated

474
Q

UTIs IN PREGNANCY
what are the signs and symptoms?

A
  • typical UTI symptoms = frequency, dysuria
  • cystitis = urgency, frequency, dysuria, hematuria, proteinuria, suprapubic pain
  • Pyelonephritis = fever, rigors, loin pain (also hyperemesis or preterm labor)
475
Q

UTIs IN PREGNANCY
what are the investigations?

A
  • Urine analysis (nitrities and leukocytes)
  • MSU
  • Bloods
  • Renal USS
476
Q

UTIs IN PREGNANCY
what are the treatments?

A
  • Oral antibiotics
    - Asymptomatic bacteriuria: 3 days
    - Cystitis 7 days
477
Q

UTIs IN PREGNANCY
what is the management of pyelonephritis?

A

antibiotics (IV) for 10-14 days
- Pyelonephritis needs IV antibiotics until pyrexia settles and vomiting stops. IV fluids and antipyretics too.

478
Q

UTIs IN PREGNANCY
how can UTIs be prevented?

A
  • Increase fluid intake
  • Double voiding and emptying bladder after sex
  • Cranberry juice
  • Prophylactic antibiotics
479
Q

UTIs IN PREGNANCY
what are the antenatal risk factors for UTIs?

A
  • previous infection
  • renal stones
  • diabetes mellitus
  • immunosuppression
  • polycystic kidneys
  • congenital abnormalites of renal tract
  • neuropathic bladder
480
Q

UTIs IN PREGNANCY
what are the postpartum risk factors?

A

the risk is mainly associated with catheterisation
- prolonged labour
- prolonged 2nd stage
- C-section
- pre-eclampsia

481
Q

UTIs IN PREGNANCY
what is the management?

A

antibiotics (depends on sensitivities)
- penicillin amoxicillin
- cephalosporin
- gentamycin (have to monitor levels to minimise risk of ototoxicity)

482
Q

UTIs IN PREGNANCY
which antibiotics should be avoided in first trimester and why?

A

trimethoprim
it is a folate antagonist so can reduce folate levels

483
Q

UTIs IN PREGNANCY
which antibiotics should be avoided in the third trimester and why?

A
  • nitrofurantoin - risk of haemolytic anaemia in newborn with G6PD
  • sulfonamides - risk of kernicterus in newborn due to displacement of protein binding of bilirubin
484
Q

UTIs IN PREGNANCY
which antibiotics are contraindicated in pregnancy?

A
  • tetracyclines - cause permanent staining of teeth and problems with skeletal development
  • ciprofloxacin - causes skeletal problems
485
Q

CEPHALOPELVIC DISPROPORTION
what is it?

A

a rare complication of birth where the baby’s head does not clear the opening of the pelvis

486
Q

CEPHALOPELVIC DISPROPORTION
what are the neonatal factors that may cause it?

A
  • large baby size due to:
    - past due date
    - excessive maternal weight gain during pregnancy
    - FHx of large babies
    - gestational diabets
    - multiparity
    - parents are obese
487
Q

CEPHALOPELVIC DISPROPORTION
what are the maternal factors that may cause it?

A
  • small pelvis due to:
    - birthing in adolescence
    - pelvic malformations (bony growths)
    - petite birthing parent
    - previous trauma e.g. fractured pelvis
488
Q

CEPHALOPELVIC DISPROPORTION
what can increase the risk?

A
  • flat (platypelloid) pelvic opening
  • heart-shaped (android) pelvis
489
Q

CEPHALOPELVIC DISPROPORTION
what are the signs and symptoms?

A
  • failure to progress
    - 1st labour and last >20hrs
    - previously given birth and lasts >14hrs
  • baby’s head is not moving towards pelvic opening
  • contractions aren’t strong enough to move baby along birth canal
  • slow/no thinning or dilation of cervix
490
Q

CEPHALOPELVIC DISPROPORTION
how is it diagnosed?

A
  • check cervix to see if it is opening
  • foetal monitor to assess contractions
  • palpate abdomen to assess foetal position
  • can be diagnosed via USS if baby is growing fast
491
Q

CEPHALOPELVIC DISPROPORTION
what is the management?

A
  • vacuum extraction or forceps
  • c-section
492
Q

CEPHALOPELVIC DISPROPORTION
what are the complications?

A
  • shoulder dystocia
  • vaginal tears
  • postpartum haemorrhage