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Phase 3a Revision > OBS > Flashcards

OBS 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 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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17
Q

MISCARRIAGE
What is the most common cause of miscarriage in the second trimester?
What are some risk factors?

A
  • Incompetent cervix

- Previous cervical surgery, BV in 2nd trimester

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18
Q

MISCARRIAGE

What are some other causes of miscarriage?

A
  • PCOS
  • TORCH infections
  • Iatrogenic (amniocentesis, CVS)
  • Smoking, substance abuse
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19
Q

MISCARRIAGE

What are the 6 types of miscarriage?

A
  • Threatened
  • Inevitable
  • Incomplete
  • Complete
  • Missed
  • Septic
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20
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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21
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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22
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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23
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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24
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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25
Q

MISCARRIAGE

What is a blighted ovum?

A
  • In missed miscarriage, a gestational sac >25mm but no embryonic/foetal pole
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26
Q

MISCARRIAGE

What is a septic miscarriage?

A
  • Contents of uterus infected causing endometritis
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27
Q

MISCARRIAGE
What is a…

i) pregnancy of uncertain viability?
ii) pregnancy of unknown location?

A

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

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

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28
Q

MISCARRIAGE

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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29
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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30
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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31
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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32
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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33
Q

MISCARRIAGE

What are the risks of expectant and medical management?

A
  • Bleeding continuing
  • Increased pain
  • Infected POC
  • Failure
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34
Q

MISCARRIAGE

What are some indications for surgical management?

A
  • Heavy bleeding
  • Infection
  • Failed other methods
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35
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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36
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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37
Q

MISCARRIAGE

What is a recurrent miscarriage?

A
  • ≥3 consecutive miscarriages in the first trimester with the same biological father
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38
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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39
Q

MISCARRIAGE
What is antiphospholipid syndrome?
What is the management?

A
  • Hypercoaguable state presenting with thrombosis + pregnancy issues (recurrent miscarriage)
  • Associated with antiphospholipid antibodies
  • Can occur on own or secondary to SLE
  • Low dose aspirin + LMWH
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40
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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41
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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42
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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43
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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44
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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45
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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46
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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47
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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48
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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49
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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50
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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51
Q

HYPEREMESIS
What is believed to be responsible for N+V in pregnancy? When is N+V worse?
What are some associations of hyperemesis gravidarum?

A
  • Placental beta-hCG as N+V is more severe in molar + multiple pregnancies where beta-hCG high
  • Assoc = nulliparity, hyperthyroid, obesity, decreased in smokers
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52
Q

HYPEREMESIS
What is the clinical presentation of hyperemesis gravidarum?
Complications?

A
  • Severe + excessive N+V
  • Associated with dehydration, ketosis + weight loss
  • May lead to complications like Mallory-Weiss tear
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53
Q

HYPEREMESIS
What is the diagnostic triad for hyperemesis gravidarum?
How is severity assessed?

A

Triad –
- >5% weight loss compared to before pregnancy
- Dehydration
- Electrolyte imbalance
Pregnancy-Unique Quantification of Emesis (PUQE) –
- <7 mild, 7-12 mod, >12 severe

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54
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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55
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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56
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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57
Q

HYPEREMESIS
What is the community management of hyperemesis gravidarum?
What alternative management can be used?

A
  • 1st line antiemetic = promethazine or cyclizine (anti-histamines)
  • 2nd line = ondansetron (5-HT3 antagonist) or metoclopramide (dopamine antagonist)
  • Complementary therapies like ginger or wrist acupressure
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58
Q

HYDATIDIFORM MOLE

What is a hydatidiform mole?

A
  • Part of group of rare tumours known as gestational trophoblastic disease
  • Growing mass of tissue that implants into uterus that will not come to term (non-viable fertilised egg, result of abnormal conception)
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59
Q

HYDATIDIFORM MOLE

What are the 3 types of hydatidiform mole?

A
  • Complete
  • Partial
  • Invasive
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60
Q

HYDATIDIFORM MOLE

What is a complete mole?

A
  • Diploid trophoblast cells
  • Empty egg + sperm that duplicates DNA (all genetic material comes from father)
  • No foetal tissue
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61
Q

HYDATIDIFORM MOLE

What is a partial mole?

A
  • Triploid (69XXX, 69XXY) trophoblast cells
  • 2 sperm fertilise 1 egg
  • Some recognisable foetal tissue
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62
Q

HYDATIDIFORM MOLE
What is an invasive mole?
What is the significance of this?

A
  • When a complete mole invades the myometrium

- Metaplastic potential to evolve into a choriocarcinoma

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63
Q

HYDATIDIFORM MOLE

What are some risk factors for hydatidiform mole?

A
  • Extremes of reproductive age
  • Previous molar pregnancy
  • Multiple pregnancies
  • Asian women
  • OCP
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64
Q

HYDATIDIFORM MOLE

What is the clinical presentation of hydatidiform mole?

A
  • PV bleed in first or early second trimester
  • Uterus bigger than expected for gestation
  • Severe hyperemesis
  • Early pre-eclampsia + clinical hyperthyroidism (hCG can mimic TSH)
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65
Q

HYDATIDIFORM MOLE

What are some investigations for hydatidiform mole?

A
  • Serum beta-hCG abnormally high (trophoblastic tissue producing excessive amounts > hyperemesis + thyrotoxicosis)
  • USS shows snowstorm appearance
  • Dx confirmed with histology after evacuation
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66
Q

HYDATIDIFORM MOLE

What is the main complication of hydatidiform mole?

A
  • 2-3% complete moles transition to highly malignant choriocarcinoma which can metastasise to the lungs
  • These are placental site trophoblastic tumours
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67
Q

HYDATIDIFORM MOLE

What is the management for hydatidiform mole?

A
  • Urgent referral to specialist centre
  • Complete moles = suction dilation + curettage
  • Partial moles = suction or medical evacuation
  • Invasive = suction D+C but not all removed, some resolve
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68
Q

HYDATIDIFORM MOLE

What is the management of hydatidiform mole after evacuation?

A
  • Check urinary pregnancy test in 3w – if high or mets may need chemo (cisplatin)
  • Effective contraception as advised to avoid pregnancy for 12m
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69
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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70
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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71
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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72
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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73
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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74
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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75
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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76
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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77
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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78
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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79
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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80
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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81
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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82
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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83
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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84
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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85
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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86
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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87
Q

ANTENATAL SCREENING
What is amniocentesis?
What is CVS?
What are the risks?

A
  • USS guided aspiration of some amniotic fluid, performed later in pregnancy when enough fluid to make safer
  • USS guided biopsy of placental tissue for karyotyping, performed earlier (before 15w)
  • Miscarriage, infection + failed samples
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88
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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89
Q

APH

What is an antepartum haemorrhage (APH)?

A
  • Genital tract bleeding after 24w gestation
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90
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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91
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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92
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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93
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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94
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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95
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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96
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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97
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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98
Q

PLACENTA PRAEVIA

What are some complications of placenta praevia?

A
  • PPH

- Placenta accreta or percreta

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99
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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100
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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101
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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102
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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103
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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104
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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105
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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106
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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107
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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108
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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109
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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110
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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111
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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112
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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113
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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114
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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115
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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116
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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117
Q

VASA PRAEVIA

What are some risk factors for vasa praevia?

A
  • Placenta praevia
  • Multiple pregnancy
  • IVF pregnancy
  • Bilobed placentas
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118
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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119
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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120
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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121
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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122
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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123
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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124
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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125
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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126
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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127
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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128
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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129
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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130
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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131
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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132
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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133
Q

PRE-ECLAMPSIA

What are the 2 big complications of pre-eclampsia?

A
  • Eclampsia

- HELLP syndrome

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134
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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135
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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136
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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137
Q

PRE-ECLAMPSIA
What is HELLP syndrome?
Give a specific marker other than those mentioned

A
  • Haemolysis, Elevated Liver enzymes + Low Platelets
  • Signs of liver damage + abnormalities of blood clotting
  • LDH raised in haemolysis
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138
Q

PRE-ECLAMPSIA
How does HELLP syndrome present?
Association?
How is it managed?

A
  • RUQ pain, N+V, urine tea coloured due to haemolysis
  • 10% have antiphospholipid syndrome
  • Magnesium sulfate, anti-hypertensives + deliver baby!
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139
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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140
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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141
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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142
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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143
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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144
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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145
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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146
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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147
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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148
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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149
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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150
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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151
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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152
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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153
Q

IUGR

What is low birth weight?

A
  • Baby born with a weight <2.5kg (regardless of gestational age)
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154
Q

IUGR

What are the 3 broad categories causing IUGR?

A
  • Placental insufficiency (most common cause)
  • Maternal factors
  • Foetal factors
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155
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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156
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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157
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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158
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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159
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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160
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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161
Q

IUGR

What are the investigations for IUGR?

A
  • BP + urine dipstick (?pre-eclampsia)
  • Karyotyping (?foetal)
  • Infection screen, TORCH (?infection)
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162
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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163
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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164
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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165
Q

MACROSOMIA
What is…

i) large for gestational age (LGA)?
ii) macrosomia?

A

i) Estimated foetal weight above the 90th centile for their gestational age
ii) Baby with a weight >4kg regardless of gestational age

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166
Q

MACROSOMIA

What are the causes of macrosomia?

A
  • Constitutionally large or familial (parental height + weight)
  • Maternal diabetes, previous macrosomia, obesity or rapid weight gain
  • Overdue
  • Male baby
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167
Q

MACROSOMIA

What are some complications of macrosomia?

A
  • Maternal = failure to progress, perineal tears, instrumental/c-section, PPH, uterine rupture (rare)
  • Foetal = shoulder dystocia, neonatal hypoglycaemia, obesity in childhood + later life
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168
Q

MACROSOMIA

How do you diagnose and manage macrosomia?

A
  • OGTT to screen for diabetes
  • SFH + EFW from USS to plot on growth chart + >90th centile = Dx
  • Regular growth scans to assess progress + check amniotic fluid index levels to exclude polyhydramnios
  • Most vaginal delivery, consider c-section if v large or signs of distress
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169
Q

MULTIPLE PREGNANCY
What is meant by…

i) monozygotic
ii) dizygotic
iii) mono/diamniotic
iv) mono/dichorionic

in terms of multiple pregnancy?

A

i) identical (come from single zygote)
ii) non-identical (come from two different zygotes > diamniotic + dichorionic)
iii) share/two separate amniotic sacs
iv) share/two separate placentas

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170
Q

MULTIPLE PREGNANCY
What are some predisposing factors to multiple pregnancies?
What is one way of preventing them?

A
  • Previous twins, FHx, increasing parity + maternal age, IVF, race (Afro-Caribbean)
  • No more than 2 embryos transferred per IVF cycle
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171
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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172
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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173
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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174
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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175
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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176
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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177
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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178
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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179
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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180
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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181
Q

OLIGOHYDRAMNIOS

What is the management of oligohydramnios?

A
  • Treat as PROM if present

- Frequent monitoring of growth for IUGR

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182
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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183
Q

POLYHYDRAMNIOS

What is polyhydramnios?

A
  • Abnormally large levels of amniotic fluid

- AFI >95th centile for gestational age

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184
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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185
Q

POLYHYDRAMNIOS

How may polyhydramnios present?

A
  • Maternal discomfort
  • LGA
  • Foetal parts hard to palpate
  • Taut uterus
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186
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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187
Q

POLYHYDRAMNIOS

What are some complications of polyhydramnios?

A
  • Preterm delivery
  • Malpresentation
  • Maternal discomfort from abdo distension
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188
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

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189
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

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190
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

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191
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
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192
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)
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193
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
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194
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
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195
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
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196
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
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197
Q

RHESUS DISEASE

How does anti-D work?

A
  • Immunoglobulin attaches to Rh D antigens on foetal blood in maternal circulation preventing recognition
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198
Q

CHORIOAMNIONITIS
What is chorioamnionitis?
What is a major factor in the condition?

A
  • Acute inflammation of amnion + chorion membranes due to ascending bacterial infection in setting of membrane rupture
  • PPROM
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199
Q

CHORIOAMNIONITIS

What is the clinical presentation of chorioamnionitis?

A
  • Uterine tenderness
  • Evidence of foetal distress on CTG
  • Foul odour, purulent/offensive PV discharge (yellow/brown)
  • Maternal infection (fever, abdo pain, maternal + foetal tachycardia)
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200
Q

CHORIOAMNIONITIS

What are some investigations for chorioamnionitis?

A
  • FBC, CRP (raised WCC + CRP)
  • Swabs (high + low vaginal swabs), MSU
  • USS for foetal presentation, EFW + liquor volume
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201
Q

CHORIOAMNIONITIS

What is the management of chorioamnionitis?

A
  • Steroids <34w
  • Deliver foetus (whatever gestation, often c-section)
  • IV Abx
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202
Q

GESTATIONAL DIABETES

What is Gestational Diabetes Mellitus (GDM)?

A
  • Carbohydrate intolerance during pregnancy which often resolves after birth
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203
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
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204
Q

GESTATIONAL DIABETES

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

A
  • Main one is human placental lactogen (hPL)

- Also glucagon + cortisol

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205
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
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206
Q

GESTATIONAL DIABETES

What is the clinical presentation of GDM?

A
  • May be asymptomatic or present with polydipsia, polyuria, nocturia + fatigue
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207
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
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208
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
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209
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
210
Q

GESTATIONAL DIABETES
What causes…

i) macrosomia?
ii) polyhydramnios?
iii) birth trauma?
iv) neonatal hypoglycaemia?

A

i) Excess foetal glucose > hyperinsulinaemia + so increased fat deposition
ii) Excess foetal glucose > polyuria
iii) Cephalopelvic incompatibility, shoulder dystocia
iv) Climatization + hyperinsulinaemia

211
Q

GESTATIONAL DIABETES

What are the maternal risks of GDM?

A
  • Pre-eclampsia
  • DKA or hypos
  • UTIs
  • IHD
  • Nephropathy, retinopathy
212
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
213
Q

GESTATIONAL DIABETES
What is the management of…

i) pre-existing T1DM?
ii) pre-existing T2DM?

A

i) Insulin with dose adjustment for normal changes to glucose metabolism in pregnancy
ii) Only metformin is safe, may need upgrading to insulin

214
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
215
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

216
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

217
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

218
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
219
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
220
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
221
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

222
Q

OBSTETRIC CHOLESTASIS
What is obstetric cholestasis?
What are some associations?

A
  • Intrahepatic cholestasis = reduced outflow of bile acids from liver
  • Asian women, thought to be due to increased oestrogen + progesterone levels
223
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
224
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
225
Q

OBSTETRIC CHOLESTASIS

Why can clotting be deranged in obstetric cholestasis?

A
  • Bile acids important for fat soluble vitamin absorption like vitamin K
226
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)

227
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
228
Q

INFECTIONS + PREGNANCY
What is Parvovirus?
What are the adverse effects?
What is the management?

A
  • Parvovirus B19 can give viral Sx then ‘slapped cheeks’ (erythema infectiosum)
  • Worse <20w = suppresses foetal erythropoiesis causing anaemia + foetal hydrops, death, pre-eclampsia-like (mirror) syndrome in women
  • Maternal IgM + IgG, supportive, refer to foetal medicine to monitor
229
Q

INFECTIONS + PREGNANCY
What is Group B strep (GBS) infection?
What can it cause?
How is it spread?

A
  • Strep agalactiae
  • Most common cause of early-onset severe infection (Sepsis) in neonates
  • Commonly found in maternal bowel flora
230
Q

INFECTIONS + PREGNANCY
What are the risk factors of GBS?
When should you screen?

A
  • Prematurity, prolonged ROM, previous GBS sibling, maternal pyrexia
  • If previous GBS in pregnancy either intrapartum IV Abx prophylaxis or test in late pregnancy (3-5w before EDD) + IV Abx if +ve
231
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
232
Q 
INFECTIONS + PREGNANCY
What is toxoplasmosis?
How is it spread?
What is the clinical presentation?
What is the management
A
  • Toxoplasma gondii protozoan
  • Cat poo, eating infected meat
  • Glandular fever-like illness (fever, rash, eosinophilia)
  • TORCH screen (IgM + IgG), proven infection use spiramycin
233
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

234
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
235
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

236
Q

INFECTIONS + PREGNANCY

What is the management of Hep B in pregnancy?

A
  • Babies born to Hep B +ve mothers should be vaccinated within 24h of birth as well as other times recommended on vaccination schedule
  • No breastfeeding transmission in contrast to HIV
237
Q

INFECTIONS + PREGNANCY
What are the risks of rubella in pregnancy?
What is the management?

A
  • Congenital rubella syndrome in first 8–10w (sensorineural deafness, CHD like PDA + PS, congenital cataracts, cerebral palsy)
  • Live vaccines like MMR avoided in pregnancy (offer postnatally if no immunity), avoid contacts
238
Q

INFECTIONS + PREGNANCY

What is the management of HIV in pregnancy?

A
  • Normal vaginal delivery if viral load <50 copies/ml if. not c-section (IV zidovudine 4h before)
  • Neonatal zidovudine PO if maternal viral load <50 if not triple ART, both for 4–6w
  • Breastfeeding C/I
239
Q

ANAEMIA + PREGNANCY
Why is anaemia common in pregnancy?
What are some causes?
What are some risk factors?

A
  • Hb normally falls slightly in pregnancy due to increased plasma volume diluting Hb
  • Physiological, Fe deficiency (increased demand), B12 or folate deficiency
  • Menorrhagia, malaria, hookworm, twins, poor diet
240
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
241
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
242
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.
243
Q

ASTHMA + PREGNANCY

What are the complications of asthma in pregnancy?

A
  • Foetal growth restriction due to inadequate placental perfusion
  • Premature delivery (usually due to maternal deterioration)
244
Q

ASTHMA + PREGNANCY

What is the management of asthma in pregnancy?

A
  • Optimise control pre-conception
  • All drugs for asthma safe
  • Risk of exacerbation, esp in third trimester as baby grows it can press up on lungs > in asthma attack, prioritise mum
245
Q

ACUTE FATTY LIVER

What is acute fatty liver of pregnancy?

A
  • Rapid accumulation of fat within the hepatocytes that occurs in the third trimester of pregnancy
  • Rare cause of hepatitis in pregnancy
246
Q

ACUTE FATTY LIVER

What is the clinical presentation of acute fatty liver in pregnancy?

A

Vague Sx like –

  • Abdo pain
  • N+V
  • Jaundice
  • Anorexia
  • Ascites
247
Q

ACUTE FATTY LIVER

What is the management of acute fatty liver?

A
  • LFTs show elevated liver enzymes, esp. ALT

- Stabilise, admit + deliver foetus as high risk of liver failure + mortality (for both)

248
Q

THYROID + PREGNANCY
How common is hyperthyroidism in pregnancy?
How does hyperthyroidism present?
What are some complications?

A
  • Uncommon, often improves after 1st trimester
  • May present with excessive vomiting
  • Maternal = thyroid crisis with cardiac failure
  • Foetal = thyrotoxicosis due to transfer of thyroid stimulating antibodies
249
Q

THYROID + PREGNANCY

What is the management of hyperthyroidism in pregnancy?

A
  • Propylthiouracil is choice in 1st trimester (associated with maternal hepatic injury)
  • Carbimazole C/I until 2nd trimester as causes foetal abnormalities
  • If mother has stimulating antibodies, monitor foetal growth with USS
250
Q

THYROID + PREGNANCY
Is hypothyroidism in pregnancy common?
What is the prognosis of untreated hypothyroidism in pregnancy?
What is the management?

A
  • Yes
  • Early foetal loss + congenital hypothyroidism leading to impaired neurodevelopment
  • Aim for adequate replacement with levothyroxine (safe), especially in 1st trimester
251
Q

THYROID + PREGNANCY

What is post-partum thyroiditis?

A

3 stages –
- Thyrotoxicosis (3m)
- Hypothyroidism (3–6m)
- Normal thyroid function
Sx control of thyrotoxicosis, treat hypothyroidism with levothyroxine
Just need TFTs to Dx if within 12m of giving birth + Sx

252
Q

CARDIAC DISEASE

How does cardiac disease affect pregnancy?

A
  • CV disease is leading cause of indirect maternal death
  • Older women = IHD
  • Younger women = CHD that’s exacerbated in pregnancy
253
Q

CARDIAC DISEASE

What are some complications with cardiac disease in pregnancy?

A
  • Fixed output heart disease is most risky during pregnancy (AS, coarctation, prosthetic valves [anticoagulation issue], cyanosed pts)
  • Low risk cardiac conditions include AR, MR, ASD + VSD
254
Q

CARDIAC DISEASE

What is the management of cardiac disease in pregnancy where anticoagulation is needed?

A
  • Pre-conception take off warfarin + switch to LMWH like daltaparin
  • HASBLED score + predict bleeding risk as higher risk of APH + PPH
255
Q

CARDIAC DISEASE

What is the antenatal + postnatal management of cardiac disease in pregnancy?

A
  • Joint care with cardiologist, ideally with pre-pregnancy Ax
  • Prediction + prevention of heart failure (ECHO/ECG)
  • Monitor foetal growth + wellbeing
  • Timing + mode of delivery
  • Postpartum complications (cardiac failure)
256
Q

EPILEPSY + PREGNANCY

What are the complications of epilepsy in pregnancy?

A
  • Maternal = increased frequency of seizures, can lead to falls + so trauma, SUDEP (esp. if reluctant to take meds)
  • Foetal = inheritance, risk of hypoxia with maternal seizures
257
Q

EPILEPSY + PREGNANCY

What pre-conception advice should be given for women with epilepsy?

A
  • 5mg folic acid
  • Determine if medication required or if it can be rationalised
  • Aim for monotherapy > carbamazepine + lamotrigine safest
  • Valproate can cause NTD + phenytoin can cause cleft lip + palate
258
Q

EPILEPSY + PREGNANCY

What is the management of epilepsy in pregnancy?

A
  • Screen for foetal anomalies
  • Control seizures
  • Plan for delivery (avoid prolonged labour, post-partum support)
259
Q

RENAL DISEASE

What are the complications of CKD in pregnancy?

A
  • Maternal = severe HTN, worsened renal function or renal failure, pre-eclampsia
  • Foetal = premature delivery, IUGR, stillbirth, abnormalities (drug therapy)
260
Q

RENAL DISEASE
What affects the outcome of pregnancy in renal disease?
What is the pre-conceptual advice?

A
  • Degree of renal dysfunction, BP, creatinine level + proteinuria (keep high suspicion for pre-eclampsia)
  • Aspirin 75mg OD from 12w
261
Q

RENAL DISEASE
What is the management of renal disease in pregnancy?
What drugs should be used for UTI?
What drugs should be avoided in UTI?

A
  • Closely monitor renal function (U+Es, urine dipstick) + BP with regular assessment of foetal growth + wellbeing
  • Nitrofurantoin or amoxicillin
  • Trimethoprim unsafe 1st trimester (folate antagonist), nitrofurantoin unsafe in 3rd trimester (haemolytic anaemia of newborn)
262
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
263
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

264
Q

PROM

What are some risk factors for (P)PROM?

A
  • Previous PROM/preterm
  • Smoking
  • Polyhydramnios
  • Amniocentesis
265
Q

PROM

What is the clinical presentation of (P)PROM?

A
  • Gush or constant trickle or dampness from vagina

- Clear fluid

266
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)
267
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
268
Q

PROM

What are some complications of PPROM?

A
  • Risk of prematurity, chorioamnionitis, pulmonary hypoplasia
269
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)
270
Q

PREMATURITY

What are the WHO definitions of prematurity?

A
  • Birth before 37w
  • Extreme preterm = <28w
  • Very preterm = 28–32w
  • Mod-late preterm = 32–37w (term >37w)
271
Q

PREMATURITY

When are babies considered non-viable?

A
  • <24w so if no signs of life = no resus

- From 24w chances improve so full resus

272
Q

PREMATURITY

What are the classifications of prematurity?

A
  • Spontaneous (70%) = PPROM, cervical weakness, amnionitis

- Iatrogenic = induced due to some complication

273
Q

PREMATURITY

What are the risk factors of prematurity?

A
  • 50% none
  • Multiple pregnancy
  • Complications (IUGR, pre-eclampsia)
  • APH
  • Previous cervical surgery
  • Previous preterm
  • Polyhydramnios
  • Infection
  • Maternal diseases
274
Q

PREMATURITY

What is the clinical presentation of prematurity?

A
  • Persistent uterine activity WITH change in cervical dilatation ± effacement
  • Preterm labour with intact membranes if no ruptured amniotic sac
  • Increase or change in PV discharge or bleeding
275
Q

PREMATURITY

What are the investigations for prematurity?

A
  • Speculum (assess cervical dilatation, look for amniotic fluid) can Dx if <30w
  • TVS if >30w to measure cervical length (<15mm + contractions = Dx)
  • OR foetal fibronectin (Actim Partus, acts as glue between chorion + uterus + found in vagina during birth) test >50ng/ml = early labour
276
Q

PREMATURITY

What are the complications of prematurity?

A
  • Maternal = infection
  • Neonatal = necrotising enterocolitis, apneoa of prematurity, RDS, intraventricular haemorrhage, retinopathy of prematurity, jaundice, hearing issues, chronic lung disease
277
Q

PREMATURITY

What is the prophylaxis for prematurity and how do they work?

A
  • Progesterone gel or pessary decreases activity of myometrium + prevents cervix remodelling in preparation for delivery
  • Cervical cerclage = ≥1 sutures to strengthen + keep cervix closed
  • ‘Rescue’ cerclage to halt delivery
278
Q

PREMATURITY
What are the indications for…

i) progesterone prophylaxis?
ii) cervical cerclage?
iii) ‘rescue’ cerclage?

A

i) Cervical length <25mm on TVS at 16–24w
ii) Cervical length <25mm on TVS at 16–24w, previous premature birth or cervical trauma (colposcopy, cone biopsy)
iii) Cervical dilatation without ROM at 16–27+6 with no infection, bleeding or contractions

279
Q

PREMATURITY

What is the acute management of prematurity?

A
  • Senior obs + neonate input
  • Foetal monitoring (CTG)
  • Tocolytics
  • Corticosteroids
  • IV magnesium sulfate
  • Consider delayed cord clamping or cord milking (increases circulating blood volume + Hb in baby)
280
Q 
PREMATURITY
What are tocolytics?
Why are they used?
Who for?
Examples?
A
  • Drugs to delay uterine contractions
  • Administer 2x steroids or transfer to more specialist unit (with neonatal ICU)
  • Those 24–33+6w
  • CCBs like nifedipine or oxytocin receptor antagonist like atosiban if C/I, terbutaline (SABA)
281
Q

PREMATURITY
What are corticosteroids used for?
Who for?
Give examples

A
  • Aids surfactant production so helps develop + protect baby’s lungs
  • Those <34w
  • Dexamethasone, betamethasone
282
Q

PREMATURITY
What is magnesium sulfate used for?
What is the regime?

A
  • Neuroprotection + reduced risk of cerebral palsy

- Bolus + infusion for up to 24h or until birth in <34w

283
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)
284
Q

STAGES OF LABOUR

What are 7 important hormones in labour?

A
  • Prostaglandins
  • Oxytocin
  • Oestrogen
  • Beta-endorphins
  • Adrenaline
  • Prolactin
  • Relaxin
285
Q

STAGES OF LABOUR
What is the role of these hormones in labour…

i) prostaglandins?
ii) oxytocin
iii) oestrogen
iv) beta-endorphins

A

i) Aids with cervical ripening (effacement)
ii) Produced by hypothalamus, secreted by post. pituitary, surge at labour inhibits progesterone to prepare smooth muscle for uterine contractions, milk ejection reflex postpartum
iii) Surges at onset of labour to inhibit progesterone to prepare smooth muscle for labour
iv) Natural pain relief

286
Q

STAGES OF LABOUR
What is the role of these hormones in labour…

i) adrenaline?
ii) prolactin?
iii) relaxin?

A

i) Released as birth imminent to give energy
ii) Produced + secreted by ant. pituitary, allows process of milk production in mammary glands when oestrogen + progesterone decline postpartum
iii) Released from placenta to soften ligaments + cartilage of pelvis so it can expand (cervix, vaginal tissues, perineum)

287
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
288
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
289
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
290
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
291
Q

STAGES OF LABOUR
What is the difference between latent and active phase of the first stage of labour?
How quickly are women expected to dilate during the active phase?

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
  • Primis = 0.5cm/h, multiparous = 1cm/h
292
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
293
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])

294
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
295
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

296
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
297
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
298
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
299
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
300
Q

STAGES OF LABOUR

What are the 6 cardinal movements of labour?

A
  • Engagement + descent
  • Flexion
  • Internal rotation
  • Extension (crowning)
  • Restitution/external rotation
  • Expulsion
301
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
302
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
303
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
304
Q

STAGES OF LABOUR

What position is the foetal head during engagement and descent?

A
  • Occiput transverse
305
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
306
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)
307
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)
308
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)
309
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)
310
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
311
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
312
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
313
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
314
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
315
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)
316
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
317
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)
318
Q 
FAILURE TO PROGRESS
What is the process of PGE2?
What might it be used for?
What is a risk?
How to manage that risk?
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
319
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

320
Q

FAILURE TO PROGRESS

What is the aetiology of failure to progress in labour?

A
  • Power (most common)
  • Passage
  • Passenger
  • Psyche (maternal exhaustion in second stage)
321
Q

FAILURE TO PROGRESS

How can ‘power’ cause failure to progress?

A
  • Poor uterine contractions
  • Common in primigravida women
  • May need instrumental delivery or syntocinon
322
Q

FAILURE TO PROGRESS
How can ‘passage’ cause failure to progress?
What can be a consequence of this?

A
  • Inadequate pelvis, cephalopelvic disproportion
  • Obstructed labour = presenting part of foetus cannot progress into birth canal despite strong uterine contractions
  • Common in developing countries, risk of infection, fistulas
323
Q

FAILURE TO PROGRESS

How can ‘passenger’ cause failure to progress?

A
  • Size
  • Attitude
  • Lie
  • Presentation
  • Position
324
Q

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

i) size?
ii) attitude?
iii) lie?
iv) presentation?

A

i) Macrosomia, size of head as this is largest part
ii) Posture of foetus (how the back is rounded + how the head + limbs are flexed)
iii) Longitudinal, transverse, oblique
iv) Part of foetus closest to the cervix (cephalic = head first > most optimal)

325
Q

FAILURE TO PROGRESS
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
326
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)
327
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
328
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
329
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

330
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)
331
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
332
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
333
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
334
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
335
Q

BREECH

Which breech is most associated with cord prolapse and why?

A
  • Footling

- Nothing to act as plug over cervix if membranes ruptured

336
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
337
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
338
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
339
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

340
Q

FOETAL LIE
What is…

i) longitudinal lie?
ii) transverse lie?
iii) oblique lie?
iv) unstable lie?

A

i) Straight up + down
ii) Side-side, foetus perpendicular to long axis of uterus
iii) Angle
iv) Lie is actively changing (may be transverse, longitudinal, cephalic or breech)

341
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
342
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
343
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
344
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

345
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
346
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
347
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
348
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
349
Q

CTG

What does variability tell you?

A
  • Reduced variability may be hypoxia, lactic acidosis, prematurity
  • 40m reduced variability accepted as baby may be sleeping
350
Q

CTG
What are accelerations?
What do they show you?

A
  • Rise in baseline HR by 15 for ≥15s

- Reassuring as baby moving

351
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)
352
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

353
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

354
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

355
Q

CTG
What makes a CTG…

i) suspicious?
ii) pathological?

A

i) 1 non-reassuring

ii) ≥2 non-reassuring or 1 abnormal

356
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
357
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
358
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
359
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

360
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
361
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
362
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

363
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
364
Q

SHOULDER DYSTOCIA

What is shoulder dystocia?

A
  • Failure of anterior shoulder to pass under symphysis pubis after delivery of foetal head
365
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
366
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)
367
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

368
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

369
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)
370
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

371
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
372
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)
373
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
374
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
375
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 #
376
Q

INSTRUMENTAL DELIVERY

What are some maternal consequences of instrumental delivery?

A
  • Infection (co-amox stat)
  • PPH
  • Episiotomy
  • Tears
  • Incontinence
377
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
378
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
379
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
380
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
381
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
382
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)
383
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
384
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
385
Q

PAIN RELIEF

What simple analgesia can be used in labour?

A
  • Paracetamol + codeine useful in early labour

- Avoid NSAIDs

386
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
387
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)

388
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
389
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
390
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
391
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

392
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)

393
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
394
Q

PAIN RELIEF

What medications can be given epidurally?

A
  • LA like bupivacaine

- Opioids like fentanyl, diamoprhine

395
Q

PAIN RELIEF

What sequential effects do regional techniques have?

A
  • Autonomic (vasodilation = reduced MAP)
  • Sensory (analgesia)
  • Motor (motor blockade) + fever
396
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
397
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
398
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
399
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
400
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
401
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
402
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
403
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
404
Q

PERINEAL TEARS

What are some risk factors for perineal tears?

A
  • Primigravida
  • Macrosomia
  • Shoulder dystocia
  • Forceps
405
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
406
Q

PROLONGED PREGNANCY
What is a prolonged pregnancy?
What are some investigations?

A
  • Pregnancy exceeding 42w from LMP
  • USS assessment of growth + amniotic fluid volume
  • Daily CTGs after 42w + Advised to report any decreased foetal movements
407
Q

PROLONGED PREGNANCY

What are some complications of prolonged pregnancy for the foetus?

A
  • Macrosomia (+ dystocia)
  • Oligohydramnios
  • Reduced placental perfusion
  • May have meconium stained liquor (foetal distress), beware of aspiration as can cause severe pneumonitis
408
Q

PROLONGED PREGNANCY
What are the maternal complications of prolonged pregnancy?
What is the management?

A
  • Anxiety, more interventions (induction, operative delivery)
  • Confirm EDD, offer one membrane sweep at 41w + induction at 41–42w to prevent this
409
Q

UTERINE RUPTURE
What is a uterine rupture?
What are the two types?
What is the risk?

A
  • Complication of labour where myometrium bursts
  • Incomplete = peritoneal lining surrounding uterus intact
  • Complete = peritoneal lining ruptures so uterine contents released into peritoneal cavity
  • Significant haemorrhage, high morbidity + mortality for baby + mother
410
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
411
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
412
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
413
Q

AMNIOTIC EMBOLISM

What is an amniotic fluid embolism?

A
  • Amniotic fluid/foetal cells enter mother’s blood stream causing an immune reaction from the mother’s immune system > systemic illness
414
Q

AMNIOTIC EMBOLISM
What are some risk factors for amniotic fluid embolism?
Presentation?

A
  • Increasing maternal age + ARM
  • Often around time of labour + delivery but can be postpartum
  • Sx = SOB, sweating, anxiety, seizures, haemorrhage
  • Signs = hypoxia, tachycardia + hypotension, may lead to cardiac arrest
415
Q

AMNIOTIC EMBOLISM

What is the management of amniotic fluid embolism?

A
  • Supportive + requires involvement from critical care (maternal A-E resus)
416
Q

PPH
What is a postpartum haemorrhage (PPH)?
What are the classifications?

A

Primary = loss of >500ml blood in the first 24h after delivery
- Minor = 500–1000ml estimated blood loss
- Major = >1000ml, clinically in shock
Secondary = excessive blood loss from genital tract between 24h–12w after delivery (can result in Sheehan’s syndrome)

417
Q

PPH

What are the 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)
Secondary most common cause is retained placental tissue, endometritis

418
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
419
Q

PPH

How might uterine atony present in PPH?

A
  • Unpalpable uterus on abdo exam (should normally be palpable in period following birth)
420
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
421
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
422
Q

PPH

What mechanical treatment can be trialled in PPH?

A
  • Rub uterus through abdomen to stimulate contraction
423
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)
424
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)
425
Q

MATERNAL SEPSIS
What is sepsis?
What is septic shock?
What is the importance of sepsis?

A
  • Life-threatening organ dysfunction from dysregulated host response to infection
  • Persistent tissue hypoperfusion despite adequate fluid replacement
  • One of top direct causes of maternal death in UK
426
Q

MATERNAL SEPSIS

What are some causes of sepsis?

A
  • Pyelonephritis
  • Chorioamnionitis
  • Wound infection (c-section, episiotomy)
  • GBS
  • Pneumonia
  • Cellulitis
  • Basically any infection
427
Q

MATERNAL SEPSIS

What are some risk factors for sepsis?

A
  • Immunosuppressed
  • Obesity
  • DM
  • Hx of pelvic infection
  • Amniocentesis + CVS
  • Cervical stitch
  • Prolonged ROM (>18h in prems, >24h in term)
428
Q

MATERNAL SEPSIS

What is the clinical presentation of sepsis?

A
  • Pyrexia OR hypothermia, rigors, non-blanching rash
  • Tachycardia + hypotension (shock)
  • Oliguria, hypoxia, impaired consciousness
  • Failure to respond to treatment
429
Q

MATERNAL SEPSIS

What are the investigations for maternal sepsis?

A
  • Monitor Maternal Early Obstetric Warning Score (MEOWS)

- Warning signs of sepsis (3Ts white with sugar)

430
Q

MATERNAL SEPSIS

What are the warning signs of sepsis?

A

3Ts white with sugar –

  • Temp <36 or >38
  • Tachycardia >90bpm
  • Tachypnoea >20bpm
  • WCC >12 or <4
  • Hyperglycaemia >7.7mmol/L in absence of diabetes
431
Q

MATERNAL SEPSIS

How can maternal sepsis be prevented?

A
  • All pregnant ladies get seasonal flu vaccine
  • Broad-spec IV Abx then alter with sensitivities
  • Involve senior team + experts early
  • SEPSIS 6 within first hour
  • Consider delivery + VTE prophylaxis
432
Q

MATERNAL SEPSIS

What are the SEPSIS 6 components?

A

BUFALO (3 in, 3 out) –

  • Blood cultures (out)
  • Urine output by catheter (hourly, out)
  • Fluids resus (IV, in)
  • Abx (IV broad-spec, in)
  • Lactate (ABG, out)
  • Oxygen (high flow SpO2 >94%, in)
433
Q

MATERNAL SEPSIS
What is puerperal pyrexia?
What are the causes?
What is the management

A
  • Temp >38 in first 14d postpartum
  • Endometritis #1, UTI, mastitis, wound infections, VTE
  • Endometritis = hospital for IV Abx (clindamycin/gent) until afebrile >24h
434
Q

MATERNAL SEPSIS
What is the clinical presentation of endometritis?
What can cause it?
How should you investigate it?

A
  • Foul-smelling discharge or lochia, bleeding gets heavier or does not improve with time, lower abdo pain
  • Commonly after c-section (give prophylactic Abx), can be caused by STIs
  • Vaginal swabs + urine MC&S
435
Q

NEWBORN SCREENING

What types of newborn screening are there?

A
  • Newborn infant physical examination (NIPE)
  • Newborn blood spot conditions
  • Newborn hearing screen
436
Q

NEWBORN SCREENING
When is the NIPE done?
What for?

A
  • First within 72h of birth + Second by GP at 6–8w

- Screens for problems with hips, eyes, heart + genitalia

437
Q

NEWBORN SCREENING

What is the process of the newborn blood spot conditions screen (Guthrie/heel-prick)?

A
  • Screening on day 5–9

- Residual blood spots stored for 5 years (part of consent process) for research

438
Q

NEWBORN SCREENING

What conditions does the newborn blood spot screen for?

A 
3 genetic –
- Sickle cell disease
- Cystic fibrosis
- Congenital hypothyroidism
6 inherited metabolic –
- Phenylketonuria
- Medium-chain acyl-CoA dehydrogenase deficiency 
- Maple syrup urine disease
- Isovaleric acidaemia
- Glutaric aciduria type 1
- Homocystinuria
439
Q

NEWBORN SCREENING
What is the rough incidence of…

i) sickle cell disease?
ii) cystic fibrosis?
iii) congenital hypothyroidism?
iv) phenylketonuria?
v) MCADD?
vi) MSUD?
vii) IVA?
viii) GA1?
ix) homocystinuria?

A

i) 1 in 2000
ii) 1 in 2500
iii) 1 in 3000
iv) 1 in 10,000
v) 1 in 10,000
vi) 1 in 150,000
vii) 1 in 150,000
viii) 1 in 300,000
ix) 1 in 300,000

440
Q

NEWBORN SCREENING
What specifically is tested for in…

i) cystic fibrosis?
ii) congenital hypothyroidism?
iii) phenylketonuria?

A

i) Immunoreactive trypsinogen
ii) TSH
iii) Phenylalanine

441
Q

NEWBORN SCREENING
What is phenylketonuria?
What are the features of phenylketonuria?
What is the management?

A
  • AR defect in phenylalanine hydroxylase (C12)
  • LDs, seizures, ‘musty’ odour to urine + sweat, (fair hair, blue eyes)
  • Phenylalanine restricted diet
442
Q

NEWBORN SCREENING

What is the management of MCADD?

A
  • Avoid long periods with no food

- High sugar drinks when ill

443
Q

NEWBORN SCREENING
What does MSUD, IVA and GA1 have in common?
What are their differences?
What is the management?

A
  • Issues with processing amino acids
  • MSUD = leucine, isolecine + valine
  • IVA1 = leucine
  • GA1 = lysine, hydroxylysine + tryptophan
  • Limit high protein foods
444
Q

NEWBORN SCREENING
What is homocystinuria?
How does it present?
What is the management?

A
  • Cystathionine synthetase deficiency
  • Developmental delay, MSK like Marfan, fair complexion, brittle hair, dislocation of lens
  • Pyridoxine (vitamin B6)
445
Q

NEWBORN SCREENING
What is the newborn hearing screening?
Why is it done?

A
  • All babies screened within 4w of birth ideally (up to 3m)

- Early identification crucial for developing speech, language + social skills

446
Q

NEWBORN SCREENING
What does the newborn hearing screen involve?
What is the outcome?

A
  • Automated otoacoustic emission (AOAE) test with some babies needing automated auditory brainstem response (AABR) test
  • Refer to audiology within 4w if no clear response with one or both ears
447
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
448
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
449
Q

MENTAL HEALTH
What are baby blues?
How common is it?
What is the management?

A
  • Brief period of tearfulness, anxiety + emotional lability starting 3–10d after birth
  • Affects up to 70% of women, classically primiparous
  • Reassure natural to feel emotional + overwhelmed, health visitor obs
450
Q

MENTAL HEALTH
What is postnatal depression?
What are some risk factors?

A
  • Depressive episode, temporally related to childbirth, within 6m post-partum
  • Risk factors = PMH/FHx of MH issues, Hx of abuse, lack of support/relationships, low socioeconomic status, unemployed
451
Q

MENTAL HEALTH
What can be used to measure postnatal depression?
How does postnatal depression present?

A
  • Edinburgh postnatal depression scale = screening tool, >10 suspect
  • Typical depression Sx but may include worries about baby’s health or ability to cope adequately, feeling detached from the baby
452
Q

MENTAL HEALTH

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
453
Q

MENTAL HEALTH
What is postpartum/puerperal psychosis?
What are some risk factors?

A
  • Acute psychotic episode with peak occurrence at 2w postpartum
  • FHx/PMH of MH (esp. postpartum psychosis), traumatic birth or pregnancy, primiparous
454
Q

MENTAL HEALTH

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
455
Q

MENTAL HEALTH

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
456
Q

PUERPERIUM
What is the puerperium?
What does it involve?

A
  • Delivery of placenta to 6w following birth

- Return to pre-pregnant state, initiation/suppression of lactation + transition to parenthood

457
Q

PUERPERIUM

What is the postnatal period?

A
  • Period under which woman + baby are still under midwife care, usually at least 10d + for as long as midwife feels necessary
458
Q

PUERPERIUM
What is…

i) maternal death?
ii) direct maternal death?
iii) indirect maternal death?

A

i) Death of a woman during or up to 6w after her pregnancy (may or not have been aggravated by pregnancy)
ii) Mother dying as a result of an obstetric complication
iii) Mother dying as a result of a pre-existing disease or disease that developed during pregnancy, but not as a direct obstetric cause

459
Q

PUERPERIUM

What are some direct and indirect causes of maternal death?

A
  • Direct = VTE (#1), haemorrhage, HTN disorders, suicide

- Indirect = cardiac disease

460
Q

PUERPERIUM

What are some major and minor post-natal problems?

A
  • Major = sepsis, PPH, pre-eclampsia, VTE, uterine prolapse, breast abscess, MH issues
  • Minor = fatigue, anaemia, mastitis, baby blues
461
Q

PUERPERIUM

What changes happen during the puerperium?

A
  • Big decrease in serum placental hormones (hPL, hCG, oestrogen + progesterone)
  • Uterus involutes from 1kg > 100g + cervix firm after 3d
  • Decidua is shed as lochia
  • Milk replaces colostrum after 3d
  • Breast engorgement (swollen, red + tender) after 3d
462
Q

PUERPERIUM

What are the different types of lochia?

A
  • Rubra (red) 0–4d (blood cervical discharge, meconium)
  • Serosa (yellow) 4–10d (mucus, exudate, foetal membrane, WBCs)
  • Alba (white) 10–28d (cholesterol, fat, leukocytes, mucus)
463
Q

PUERPERIUM

What is the difference between colostrum and breast milk?

A
  • Colostrum at birth = yellow fluid, first form of milk with high proteins (IgA, lactoferrin), low sugar + fat
  • Milk = lactose, protein, fat + water
464
Q

PUERPERIUM

What is the physiology of breast feeding?

A
  • Baby suckles so sensory impulses from nipple > brain
  • Prolactin secreted by ant. pit > breasts via blood + lactocytes produce milk
  • Oxytocin secreted by post. pit > breasts via blood causes myometrial cell contraction to expel milk
465
Q

PUERPERIUM

When else is prolactin secreted and why?

A
  • More at night
  • Suppresses ovulation
  • Levels peak after feed to produce more for next feed
466
Q

PUERPERIUM
What stimulates oxytocin secretion?
What hinders it?

A
  • Sight, sound + smell of baby (conditioned over time)

- Hindered by anxiety, stress + pain

467
Q

PUERPERIUM

What is lactoferrin?

A
  • Multifunctional protein in milk but loads in colostrum
  • Regulates iron absorption in intestines + delivery of iron to cells
  • Prevention against infections
  • Regulation of bone marrow function + boosts immune system
468
Q

PUERPERIUM

What are some drug contraindications in breastfeeding?

A
  • Abx (ciprofloxacin, tetracyclines, chloramphenicol)
  • Psych drugs (lithium, BDZs)
  • Amiodarone, aspirin
  • Carbimazole, methotrexate
  • Sulfonylureas
  • Cytotoxic drugs
469
Q

PUERPERIUM

What are the pros + cons of breast feeding?

A
  • Readily available good nutrition, cheaper, contraceptive effect, decrease childhood infections (gastroenteritis), decrease in necrotising enterocolitis
  • Feed more often, uncomfortable + pain (mastitis)
470
Q

PUERPERIUM

What contraception can be offered to women?

A
  • POP + implant safe in breastfeeding, start any time
  • COCP UKMEC4 <6w + UKMEC2 >6w, avoid in breastfeeding
  • IUD/IUS inserted <48h OR >4w but is UKMEC3 between
471
Q

PUERPERIUM
What is mastitis?
What can cause it?

A
  • Inflammation of breast tissue
  • Obstruction of ducts + accumulation of milk (prevent by expressing regularly)
  • Infection enter at nipple>duct (commonly S. aureus)
472
Q

PUERPERIUM
How does mastitis present?
What can it lead to?

A
  • Breast pain + tenderness, erythema, local inflammation

- Breast abscess if untreated

473
Q

PUERPERIUM
How does breast abscess present?
What is the management?

A
  • Unilateral erythema, tenderness, fever, palpable mass + tender/enlarged LNs in axilla
  • Requires surgical incision + drainage
474
Q

PUERPERIUM

What is the management of mastitis?

A
  • Milk MC&S if ?infection
  • Analgesia
  • Continue feeding or expressing
  • Flucloxacillin 10–14d if systemically unwell, nipple fissure, Sx>24h, infection
475
Q

SHEEHAN’S SYNDROME

What is Sheehan’s syndrome?

A
  • Drop in circulating blood volume leads to avascular necrosis of the pituitary gland
  • Ischaemia + infarction of anterior pituitary cells as supplied by hypothalamo-hypophysial portal system which is susceptible to rapid drops in BP after PPH
476
Q

SHEEHAN’S SYNDROME
How does Sheehan’s syndrome present?
What is the management?

A
  • Reduced lactation (lack of prolactin)
  • Amenorrhoea (lack of LH + FSH > HRT)
  • Hypothyroidism (lack of TSH > levothyroxine)
  • Adrenal insufficiency (lack of ACTH > hydrocortisone)
477
Q

PREGNANCY PHYSIOLOGY

What hormones increase in regards to the anterior pituitary gland?

A
  • ACTH = rise in steroid hormones (cortisol, aldosterone) = improves autoimmune conditions (RA) but susceptible to DM + infections
  • Prolactin = suppresses FSH + LH
  • Melanocyte stimulating hormone = increased skin pigmentation (linea nigra + melasma = brown pigmentation)
478
Q

PREGNANCY PHYSIOLOGY

What other hormones rise in pregnancy?

A
  • T3/T4
  • HCG = doubles every 48h until plateau at 8–12w then gradual fall
  • Progesterone
  • Oestrogen
479
Q

PREGNANCY PHYSIOLOGY

What changes occur to the uterus in pregnancy?

A
  • Increase from 100g–1.1kg
  • Hyperplasia + hypertrophy of myometrium
  • Decidual spiral arteries remodelled for wide bore low resistance
480
Q

PREGNANCY PHYSIOLOGY

What changes occur to the cervix in pregnancy?

A
  • Increased oestrogen = ?cervical ectropion + increased discharge
  • Before delivery, prostaglandins break down collagen in cervix = dilate + efface
  • Chadwick’s sign = early pooled deoxygenated blood > blue tinge
481
Q

PREGNANCY PHYSIOLOGY

What changes occur to the vagina in pregnancy?

A
  • Oestrogen > hypertrophy of vaginal muscles + increased PV discharge
  • Makes bacterial + candida infection more common
482
Q

PREGNANCY PHYSIOLOGY

What changes occur to the breasts?

A
  • Increased size with increased gestation

- Fat deposition around gland tissue

483
Q

PREGNANCY PHYSIOLOGY
In terms of the cardiovascular system in pregnancy, what…

i) increases?
ii) decreases?

A

i) Blood volume, plasma volume, CO (as increased SV + HR)
ii) Peripheral vascular resistance (can cause flushing + hot sweats) + BP in early-mid pregnancy but returns to normal by term

484
Q

PREGNANCY PHYSIOLOGY

What changes can occur to the vascular system?

A
  • Varicose veins due to peripheral vasodilation + obstruction of IVC by uterus
485
Q

PREGNANCY PHYSIOLOGY

What CVS anatomical changes are there?

A
  • Diaphragmatic elevation > heart displaced upwards/left so apex moved laterally
  • Increased ventricular muscle mass + increased LV/LA size
  • Altered QRS (LAD), ECG changes (inverted T waves) + flow (ES) murmurs
486
Q

PREGNANCY PHYSIOLOGY

In terms of the respiratory system, what are the mechanical changes?

A
  • Increased subcostal angle, pulmonary blood flow + tidal volume
  • Decreased vital capacity + functional residual capacity
  • Progesterone causes trachea-bronchial smooth muscle relaxation
487
Q

PREGNANCY PHYSIOLOGY

In terms of the respiratory system, what are the biochemical changes?

A
  • Increased oxygen consumption (20%) + RR
  • Compensated resp alkalosis may occur as increased pO2 + reduced pCO2 (facilitates foetal CO2 excretion), renal HCO3- excretion to prevent this
  • Increased 2,3 DPG to promote maternal Hb to release oxygen
488
Q

PREGNANCY PHYSIOLOGY
In terms of the renal system, what…

i) increases?
ii) decreases?

A

i) Blood flow to kidneys (so GFR), aldosterone (Na + water reabsorption + Retention), protein excretion
ii) Serum creatinine, urate + albumin

489
Q

PREGNANCY PHYSIOLOGY
What can happen in terms of the urinary system?
What is a consequence of this?
What else contributes?

A
  • Dilatation of ureters + collecting system > physiological hydronephrosis (more R)
  • Increased risk of UTIs
  • Decreased ureter tone/peristalsis = urinary stasis
490
Q

PREGNANCY PHYSIOLOGY

What 4 forces/pressures govern fluid retention in pregnancy?

A
  • Capillary (hydrostatic) pressure of blood in vessel = draws fluid OUT
  • Interstitial fluid colloid oncotic pressure of proteins in interstitial fluid = draws fluid OUT
  • Interstitial fluid pressure of tissues surrounding vessel = draws fluid IN
  • Plasma colloid oncotic pressure (albumin) = draws fluid IN
491
Q

PREGNANCY PHYSIOLOGY
Why does pregnancy cause dilutional anaemia?
What is the purpose of this?

A
  • Increased RBC production = higher iron, folate + B12 requirements
  • Increased ECF + plasma volume MORE than RBC volume leading to lower red cell conc (haematocrit) + lower Hb conc
  • Facilitates placental perfusion
492
Q

PREGNANCY PHYSIOLOGY

What happens in terms of clotting in pregnancy?

A
  • Clotting factors (fibrinogen, VII, VIII + X) increase
  • Plasminogen activator inhibitor increases (plasmin usually breaks clots down)
  • Hypercoaguable state
493
Q

PREGNANCY PHYSIOLOGY
In terms of haematology in pregnancy, what…

i) increases?
ii) decreases?

A

i) WBCs, ESR, d-dimers, ALP

ii) Platelets, albumin

494
Q

PREGNANCY PHYSIOLOGY

What are the metabolic changes are there in pregnancy?

A
  • Early = post-prandial glucose plasma peak lower due to fat deposition + glycogen storage
  • Late = higher for longer + maternal insulin resistance (via hPL) for foetal glucose sparing
  • Maternal insulin rises during most of pregnancy
495
Q

PREGNANCY PHYSIOLOGY

What are the changes to the skin and hair in pregnancy?

A
  • Linea nigra + melasma
  • Striae gravidarum
  • General pruritus (?OC)
  • Spider naevi + palmar erythema
  • PP hair loss normal, improves within 6m
496
Q

PREGNANCY PHYSIOLOGY

What facilitates blastocyst implantation in pregnancy?

A
  • Increased GFs, proteolytic enzymes + inflammatory mediators
  • Not rejected as change in self/non-self pattern recognition molecules (HLA + MHC proteins)
497
Q

PREGNANCY PHYSIOLOGY

In pregnancy, what changes to the humoral and cell-mediated immunity?

A
  • Humoral = unchanged, plenty of circulating Th2 cells to fight infections (antibodies)
  • Cell-mediated = reduced as progesterone down regulates production of Th1 cells (phagocytes, cytotoxic T lymphocytes)
498
Q

PREGNANCY PHYSIOLOGY
What is the impact of dampening Th1 production?
What are the implications?

A
  • Shift to increased Th2 production (bias) to protect foetus

- Pre-eclampsia, IUGR + miscarriage do not have a Th2 bias

499
Q

REPRODUCTION

What are the different stages in follicular genesis and what stage in the cell cycle are they?

A
  • Primordial follicles = diploid, arrested at prophase I
  • Primary follicle = diploid, undergoing meiosis I
  • Secondary follicle = haploid, once meiosis I complete
  • Antral (Graafian) follicle = haploid, frozen in metaphase II
500
Q

REPRODUCTION
What are the structures of…

i) primordial follicles?
ii) primary follicles?

A

i) Each contain primary oocyte (germ cells) that eventually form mature ovum
ii) Primary oocyte > zona pellucida > cuboidal granulosa cells, zona pellucida secreted from granulosa cells

501
Q

REPRODUCTION

What happens when follicles reach the secondary follicle stage?

A
  • Granulosa cells express FSH receptors = oestrogen production to grow
  • Theca cells express LH receptors = steroidogenesis
502
Q

REPRODUCTION

How is a dominant follicle chosen?

A
  • Fluid-filled chamber (antrum) starts to develop causing rapid growth
  • Rising LH leads to rising oestrogen
  • Dominant follicle with lots of FSH receptors outgrows the others
503
Q

REPRODUCTION

What happens at ovulation?

A
  • LH surge = smooth muscle of theca externa contracts
  • Follicle bursts + secretes enzymes puncturing hole in ovary
  • Fimbriae of fallopian tubes sweeps oocyte up, surrounded by zona pellucida
  • Leftover follicle > corpus luteum
504
Q

REPRODUCTION

How does fertilisation occur?

A
  • Sperm enters fallopian tube + attempts to penetrate through corona radiata + zona pellucida via acrosome reaction
  • Fusion of sperm + egg = zygote
505
Q

REPRODUCTION

What happens immediately after fertilisation?

A
  • Cell rapidly divides > mass of cells (morula) travels to uterus
  • Fluid filled cavity (blastocele) expands to form blastocyst (>80 cells) with outer layer (trophoblast) + inner layer (embryoblast)
506
Q

REPRODUCTION
When does the blastocyst reach the uterus?
What happens?

A
  • 8–10d after ovulation
  • Trophoblast cells undergo adhesion to stroma of endometrium
  • Outer layer of trophoblast (syncytiotrophoblast) forms projections into the stroma
507
Q

REPRODUCTION
Once the blastocyst has implanted, what happens to the stroma?
What signifies blastocyst implantation?

A
  • Cells of stroma convert into decidua to provide nutrients (decidual reaction)
  • Syncytiotrophoblast produces hCG to maintain corpus luteum
508
Q

REPRODUCTION

What happens to the embryoblast after implantation?

A
  • Divides into yolk sac + amniotic cavity on opposing sides with embryonic disc between
  • Chorion surrounds this complex with inner cytotrophoblast + outer syncytiotrophoblast which is embedded in endometrium
509
Q

REPRODUCTION

How does the chorion develop over time?

A
  • Chorionic cavity forms around the yolk sac, embryonic disc + amniotic sac + these structures suspended from the chorion by the connecting stalk (eventually umbilical cord)
510
Q

REPRODUCTION
When does the embryonic disc develop further?
What does it develop into?

A
  • 5w

- Foetal pole with 3 layers = ectoderm (outer), mesoderm (mid), endoderm (inner)

511
Q

REPRODUCTION
What tissues does the…

i) ectoderm
ii) mesoderm
iii) endoderm

produce?

A

i) Skin, hair, nails, teeth, CNS
ii) Heart, muscle, bone, connective tissue, kidneys, blood
iii) GI tract, lungs, liver, pancreas, thyroid, reproductive

512
Q

REPRODUCTION

When do actual organs begin to develop?

A
  • 6w foetal heart forms + starts to beat

- 8w all major organs start development

513
Q

REPRODUCTION

How does the placenta develop?

A
  • Syncytiotrophoblast forms chorionic villi with foetal blood vessels
  • Those nearest connecting stalk most vascular, cells proliferate + become placenta at about 10w
514
Q

REPRODUCTION

How is nutrient diffusion facilitated in terms of how the placenta develops?

A
  • Spiral arteries reduce their vascular resistance (narrow bore high resistance > wide bore low)
  • Makes them more fragile so blood flows out causing pools of blood (lacunae) at 20w surrounding chorionic villi for diffusion
515
Q

REPRODUCTION

What role does the placenta play in immunity?

A
  • IgG crosses placenta to give foetus immunity
  • Primary immune deficiency hypogammaglobulinaemia can occur in babies whose mothers did not have high enough IgG during pregnancy
516
Q

REPRODUCTION

What role does the placenta play in respiration?

A
  • Oxygen source for foetus, foetal Hb has higher affinity for oxygen so extracts it from maternal blood
  • CO2, H+, HCO3- + lactic acid exchanged to maintain acid-base balance
517
Q

REPRODUCTION

What role does the placenta play in nutrition and excretion?

A
  • Main source = glucose, can transfer vitamins + minerals as well as alcohol + meds
  • Similar function to kidneys, filters foetal waste (urea + creatinine)
518
Q

REPRODUCTION

What are the main hormones produced by the placenta?

A
  • hCG (maintain corpus luteum)
  • Oestrogen
  • Progesterone
  • Human placenta lactogen
519
Q

REPRODUCTION

What is the role of oestrogen in pregnancy?

A
  • Softening tissue > more flexible, allows muscles + ligaments of uterus and pelvis to expand + cervix become soft
  • Enlarges + prepares breasts + nipples for breast feeding
  • E3 declines with foetal distress, E2 increases endometrial progesterone receptors
520
Q

REPRODUCTION

What is the role of progesterone in pregnancy?

A
  • Produced by corpus luteum until 10w
  • Initially prepares endometrium for implantation by proliferation, vascularisation + decidual reaction
  • Later, maintains pregnancy by preventing contraction
  • Relaxation elsewhere > heartburn, constipation, hypotension
521
Q

REPRODUCTION

What is the role of human placental lactogen in pregnancy?

A
  • Diabetogenic as raises blood glucose levels to help increase nutrient supply + helps convert mammary glands into milk secreting tissue

Phase 3a Revision (11 decks)

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