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FINALS > Obstetrics > Flashcards

Obstetrics Flashcards

1
Q

ECTOPIC PREGNANCY
What is an ectopic pregnancy?
What is the most common site?
What is the most common site for rupture?

A
  • Implantation of a fertilised ovum outside of the uterine cavity
  • Ampulla of fallopian tube
  • Isthmus
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2
Q

ECTOPIC PREGNANCY

What are some risk factors for ectopics?

A
  • Previous ectopic (10% recurrence rate)

- Tubal damage (PID, surgery), endometriosis, IUCD, IVF, POP

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3
Q

ECTOPIC PREGNANCY

What is the clinical presentation of ectopic pregnancies?

A
  • Amenorrhoea for 6-8w
  • PV bleeding (small amount, brown)
  • Lower abdo (iliac fossa) pain (?referred shoulder tip pain if haemoperitoneum)
  • Exam = abdo tenderness, cervical motion tenderness
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4
Q

ECTOPIC PREGNANCY

What are some crucial investigations for ectopics?

A
  • EPAU = urinary beta-hCG and transvaginal USS (positive with empty uterus)
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5
Q

ECTOPIC PREGNANCY

What are the 3 management options for ectopics and their criteria?

A
  • Expectant = size <35mm, unruptured, no Sx, no foetal heartbeat, hCG <1000
  • Medical = size <35mm, unruptured, no major pain, no foetal heartbeat, hCG <5000
  • Surgical = size ≥35mm, ruptured, pain, visible foetal heartbeat, hCG >5000
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6
Q

ECTOPIC PREGNANCY

What is expectant management of ectopics?

A
  • Effectively do nothing

- Requires serial serum hCG to ensure dropping (must return for follow up)

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7
Q

ECTOPIC PREGNANCY

What is medical management of ectopics?

A
  • Single dose IM 50mg/m^2 methotrexate

- Requires serial serum hCG to ensure dropping (must return for follow up)

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8
Q

ECTOPIC PREGNANCY
What is the surgical management of ectopics?
What else may be required?

A
  • Lap salpingectomy = contralateral tube + ovary healthy to reduce recurrence
  • Lap salpingotomy = contralateral tube defected or absent
  • Anti-D for rhesus -ve
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9
Q

MISCARRIAGE
What is a miscarriage?
What is the epidemiology?

A
  • Spontaneous termination of a pregnancy before 24w gestation
  • 15–20% of pregnancies, no increased risk after 1 but there is after 2
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10
Q

MISCARRIAGE

What are some causes of miscarriage?

A
  • 1st trimester = chromosomal abnormality (risk with increased age)
  • 2nd trimester = incompetent cervix e.g., previous cervical surgery, BV in 2nd trimester
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11
Q

MISCARRIAGE

What are the 5 types of miscarriage?

A
  • Threatened
  • Inevitable
  • Incomplete
  • Complete
  • Missed
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12
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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13
Q

MISCARRIAGE

What is an inevitable miscarriage?

A
  • Miscarriage will occur
  • Heavy PV bleed with clots + crampy abdo pain with open cervical os
  • TVS = intrauterine pregnancy
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14
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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15
Q

MISCARRIAGE

What is a complete miscarriage?

A
  • Full miscarriage occurred with all foetal tissue passing
  • May have been alerted by pain + bleeding, cervical os closed
  • TVS = empty uterus
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16
Q

MISCARRIAGE

What is a missed miscarriage?

A
  • Foetal tissue in utero but foetus no longer alive
  • Asymptomatic
  • TVS = non-viable intrauterine pregnancy (smaller than expected) e.g. 12w scan shows 9w foetus with no heartbeat
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17
Q

MISCARRIAGE

What is a blighted ovum?

A
  • In missed miscarriage, a gestational sac >25mm but no embryonic/foetal part
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18
Q

MISCARRIAGE
What is a pregnancy of unknown location?
What is the management?

A
  • No sign of intrauterine/ectopic pregnancy but positive beta-hCG
  • Beta-hCG >1500 = ectopic
  • If no Dx after 3 samples = expectant or methotrexate Mx
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19
Q

MISCARRIAGE

What are the investigations for miscarriage?

A
  • EPAU = speculum, serum beta-hCG (serial should double every 48h) and transvaginal USS
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20
Q

MISCARRIAGE
What is the first line management of miscarriage?
When is it not suitable?

A
  • Expectant (wait 7–14d)

- Increased haemorrhage risk, previous traumatic pregnancy experience or evidence of infection

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21
Q

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

A
  • PV misoprostol (prostaglandin analogue) with analgesia and anti-emetics
  • Contact HCP if no bleeding in 24h
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22
Q

MISCARRIAGE

What are the options for surgical management?

A
  • Vacuum aspiration (suction curettage) under local as OP

- Surgical management under general

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23
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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24
Q

MISCARRIAGE

What is a recurrent miscarriage?

A
  • ≥3 consecutive miscarriages in the first trimester with the same biological father
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25
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)
  • Endo = DM, PCOS, thyroid disease
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26
Q

MISCARRIAGE

What are the investigations for recurrent miscarriage?

A
  • Lupus anticoagulant + anti-cardiolipin antibodies
  • Thrombophilia screen
  • Pelvic USS for structural issues
  • Cytogenic analysis of POC after 3rd miscarriage
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27
Q

TERMINATING PREGNANCY

What is the legal framework for terminating pregnancies?

A
  • 1967 Abortion Act
  • 2 medical practitioners to sign legal document
  • Only registered medical practitioner can perform in licensed premise
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28
Q

TERMINATING PREGNANCY

What is the management of terminating pregnancy based on the gestation?

A
  • <9w = mifepristone (anti-progesterone) followed 48h by misoprostol
  • <13w = surgical dilation and suction of uterine contents
  • ≥15w = surgical dilation and evacuation of uterine contents or late medical abortion (mini-labour)
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29
Q

TERMINATING PREGNANCY
Where might medical termination occur?
What additional management is required after 14w?
What are some complications of termination of pregnancy?

A
  • Outpatient remotely with Marie Stopes UK
  • Cervical priming witih misoprostol or osmotic dilators
  • Infection, bleeding, pain + failure
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30
Q

TERMINATING PREGNANCY

What is the post-termination management?

A
  • Anti-D for Rh-ve women for any TOP
  • Urinary pregnancy test 3w after to confirm complete
  • Discuss contraception
  • Offer counselling
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31
Q

HYPEREMESIS GRAVIDARUM
What is hyperemesis gravidarum thought to be related to?
What are some associations?

A
  • Raised beta-hCG levels

- Multiple pregnancies, molar pregnancies, hyperthyroidism, DECREASED in smokers

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32
Q

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

A
  • Severe + excessive N+V > Mallory Weiss tear

- Associated with dehydration, ketosis + weight loss

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33
Q

HYPEREMESIS GRAVIDARUM
What is the diagnostic triad for hyperemesis gravidarum?
How is severity assessed?
What other investigations would you do?

A

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

  • Pregnancy-Unique Quantification of Emesis (PUQE)
  • Urine dipstick (ketones), MC&S (UTI), U&E
  • TV USS ?molar pregnancy
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34
Q

HYPEREMESIS GRAVIDARUM

What would warrant admission in hyperemesis gravidarum?

A
  • Unable to tolerate PO antiemetics or fluids
  • > 5% weight loss compared to before pregnancy despite anti-emetics
  • Ketones present in dipstick (++ significant)
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35
Q

HYPEREMESIS GRAVIDARUM

What is the anti-emetic management for hyperemesis gravidarum?

A
  • First line = antihistamines e.g., cyclizine, promethazine
  • Second line = ondansetron, metoclopramide (<5d as EPSEs)
  • Can trial ginger and P6 wrist acupressure
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36
Q

HYPEREMESIS GRAVIDARUM

What is the general inpatient management of hyperemesis gravidarum?

A
  • VTE prophylaxis = TED stockings + LMWH
  • Monitor U&Es and give IV fluids (+KCl as vomiting)
  • Vitamin supplements (incl. thiamine) to prevent Wernicke’s encephalopathy
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37
Q

GESTATIONAL TROPHOBLASTIC DISORDERS

What are the three types of gestational trophoblastic disorders and explain what they are?

A
  • Complete (hydatidiform) mole = diploid trophoblast where empty egg fertilised by single sperm which duplicates its DNA so all paternal DNA
  • Partial mole = triploid (XXX/XXY) trophoblast (2 sperm, 1 egg)
  • Invasive = complete mole invades myometrium (metaplastic potential > choriocarcinoma which metastasises to the lungs)
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38
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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39
Q

HYDATIDIFORM MOLE

What is the clinical presentation of hydatidiform mole?

A
  • PV bleed in first trimester
  • Uterus larger than expected for gestation
  • Clinical hyperemesis gravidarum and thyrotoxicosis (hCG can mimic TSH)
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40
Q

HYDATIDIFORM MOLE

What are some investigations for hydatidiform mole?

A
  • Serum beta-hCG abnormally high
  • TV USS = ‘snowstorm’ appearance with mixed echogenicity
  • Dx confirmed with histology of mole after evacuation
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41
Q

HYDATIDIFORM MOLE

What is the management for hydatidiform mole?

A
  • Urgent referral to specialist centre for suction curettage to remove
  • Surveillance = serum + urine hCG until normal
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42
Q

ANTENATAL CARE
What is meant by gravidity?
What is meant by parity?
What is the management of reduced foetal movements?

A
  • Total number of PREGNANCIES
  • Total number of BIRTHS ≥24w, regardless of foetal outcome
  • Handheld doppler for heartbeat – USS if not heard, CTG if present
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43
Q

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

A

Booking 8–12w (ideally <10w) –

  • 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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44
Q

ANTENATAL CARE
What is the recommended amount of folic acid?
What is the recommended amount of vitamin D?

A
  • ALL 400mcg
  • 5mg if – AEDs, coeliac, DM, >30kg/m^2, NTD risk
  • 10 ug
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45
Q

ANTENATAL APPTS
When is the dating scan done?
When is the anomaly scan?

A
  • Dating = 11–13+6w to confirm viability and assess for multiple pregnancy
  • Anomaly = 18–20+6
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46
Q

ANTENATAL APPTS
After the anomaly scan, routine care is given.
What is routine care and when is it given?

A
  • BP, urine dipstick and SFH ±2cm gestational age

- 25w (primis), 28w, 31w (primis), 34w, 36w, 38w, 40w (primis), 41w

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47
Q 
ANTENATAL APPTS
When is the second anaemia screen?
When do you screen for gestational diabetes?
When do you give anti-D prophylaxis?
When do you check presentation?
A
  • 28w
  • 28w
  • 28w and 34w
  • 36w = offer external cephalic version if appropriate
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48
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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49
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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50
Q

ANTENATAL SCREENING
What results indicate higher risk for…

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

A

i) >6mm
ii) Higher result
iii) Lower result (even lower for trisomy 13 + 18)

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51
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 (high)
  • Alpha-fetoprotein (low)
  • Oestriol (low)
  • Inhibin (quadruple, high)
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52
Q 
ANTENATAL SCREENING
What risk score would warrant further invasive tests?
What are those tests?
What are the risks of those tests?
What other test is available privately?
A
  • > 1:150 = screen +ve
  • Amniocentesis or chorionic villus sampling (CVS) if <15w
  • Miscarriage, infection + failed samples
  • Non-invasive prenatal testing = analyses foetal DNA in maternal blood
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53
Q

PLACENTA PRAEVIA
What is placenta praevia?
How is it graded?

A
  • Placenta is inserted wholly, or in part, into the lower segment of the uterus
  • I = reaches lower segment but not internal os
  • II = reaches internal os but doesn’t cover
  • III = covers internal os before dilation but not after
  • IV = completely covers internal os
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54
Q

PLACENTA PRAEVIA

What are some risk factors for placenta praevia?

A
  • Multiparity
  • Multiple pregnancy
  • PMHx praevia
  • Lower segment scar from c-section
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55
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 (transverse + breech)
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56
Q

PLACENTA PRAEVIA

What are the investigations for placenta praevia?

A
  • TV USS = diagnosed at 20w anomaly scan

- Rescan at 34w then 2 weekly

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57
Q

PLACENTA PRAEVIA

What is the management of asymptomatic placenta praevia?

A
  • Grade I = ?vaginal delivery

- Grade III/IV = elective c-section 37–38w but if labour starts before > crash c-section

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58
Q

PLACENTA PRAEVIA

What is the management of placenta praevia with bleeding?

A
  • ABCDE (2x large bore cannulae, X-match blood, IV fluids, senior) + admit
  • Emergency c-section if unable to stabilise or if in labour or reached term
  • Anti-D if rhesus negative
  • Maternal corticosteroids if <34w gestation
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59
Q

PLACENTAL ABRUPTION
What is placental abruption?
What are some risk factors?

A
  • Separation of a normally sited placenta from the uterine wall leading to bleeding
  • Cocaine use, pre-eclampsia, maternal smoking, trauma
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60
Q

PLACENTAL ABRUPTION

What is the clinical presentation of placental abruption?

A
  • Sudden onset severe abdo PAIN which is continuous
  • PV bleeding DARK red, shock OUT of proportion to visible loss (blood can be concealed behind placenta)
  • Maternal shock, abnormal CTG
  • Exam = tender “woody” uterus
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61
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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62
Q

PLACENTAL ABRUPTION
What is the general management of placental abruption?
How do you manage if the foetus is alive and <36w?

A
  • ABCDE (2x large bore cannulas, X-match blood, IV fluids, senior) + admit
  • Anti-D if mother Rh-ve
  • Foetal distress = immediate c-section
  • No foetal distress = admit + observe closely, corticosteroids, no tocolysis
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63
Q

PLACENTAL ABRUPTION

What is the management if the foetus is alive and >36w?

A
  • Foetal distress = immediate c-section

- No foetal distress = deliver vaginally

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64
Q

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

A
  • The chorionic villi attach to the myometrium rather than being restricted within the decidua basalis, may cause bleeding
  • Previous c-section, placenta praevia
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65
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
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66
Q

ADHERED PLACENTA

What are some complications of a morbidly adhered placenta?

A
  • Delivery risks = PPH, caesarean hysterectomy, ITU admission, infection
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67
Q

ADHERED PLACENTA

What are the investigations and management of a morbidly adhered placenta?

A
  • USS + MRI useful
  • Safest = elective c-section at 35–37w + abdominal hysterectomy
  • Can trial uterus preserving surgery or expectant but risks
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68
Q

VASA PRAEVIA
What is vasa praevia?
What are some risk factors?

A
  • Foetal vessels run near/across internal os > foetal haemorrhage
  • Placenta praevia, IVF, multiple pregnancy
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69
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) but no major maternal risk
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70
Q

VASA PRAEVIA

What is the management of vasa praevia?

A
  • Elective c-section 35–36w or if membranes rupture > emergency c-section
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71
Q

PRE-ECLAMPSIA

What is pre-eclampsia?

A
  • Pregnancy induced HTN (≥140/90) after 20w pregnancy + proteinuria (>0.3g on 24h collection or +) or evidence of other organ involvement
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72
Q

PRE-ECLAMPSIA

What is thought to be the cause of pre-eclampsia?

A
  • Abnormal development of placenta as spiral arteries do not remodel and dilate leading to placental ischaemia + endothelial cell damage
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73
Q

PRE-ECLAMPSIA

What are some high risk and moderate risk factors for pre-eclampsia?

A
  • High = previous pre-eclampsia, CKD, T1/2DM, autoimmune (SLE)
  • Moderate = first pregnancy, FHx, multiple pregnancy
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74
Q

PRE-ECLAMPSIA

What is the clinical presentation of pre-eclampsia?

A
  • Renal hypoperfusion = HTN, proteinuria + oliguria
  • Retinal hypoperfusion = blurred vision, scotomas
  • Liver = RUQ/epigastric pain
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75
Q

PRE-ECLAMPSIA

What are some signs of pre-eclampsia?

A
  • Oedema (peripheral, pulmonary and cerebral)
  • Ankle clonus = brisk reflexes NORMAL in pregnancy but not clonus
  • Papilloedema
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76
Q

PRE-ECLAMPSIA
What are the two main complications in pre-eclampsia?
What are some others?

A
  • Eclampsia + HELLP syndrome
  • Haemorrhage = DIC, stroke
  • Foetus = IUGR, prematurity
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77
Q

PRE-ECLAMPSIA
What is eclampsia?
What is the immediate seizure management?

A
  • Generalised tonic-clonic seizures in a patient with a Dx of pre-eclampsia
  • IV magnesium sulfate to prevent + treat seizures and continue for 24h after last seizure or delivery
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78
Q

PRE-ECLAMPSIA

What is the definitive management of eclampsia?

A
  • Deliver the foetus
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79
Q

PRE-ECLAMPSIA
What needs to be monitored when giving magnesium sulfate?
How is this managed?

A
  • Magnesium levels for toxicity
  • Reduced reflexes, confusion + respiratory depression
  • Calcium gluconate first line
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80
Q

PRE-ECLAMPSIA
What is HELLP syndrome?
How might is present?
What is the management?

A
  • Haemolysis (raised LDH), Elevated Liver enzymes + Low Platelets
  • RUQ pain, N+V
  • Deliver baby
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81
Q

PRE-ECLAMPSIA
What should be given to women who are at risk of pre-eclampsia?
What decides if they get it?

A
  • 75mg aspirin PO OD at 12w until birth

- ≥1 high risk factor, ≥2 moderate risk factors

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82
Q

PRE-ECLAMPSIA

What is the general management of pre-eclampsia?

A
  • Admit if BP ≥160/110mmHg
  • PO labetalol = first line (nifedipine if asthma)
  • Can trial hydralazine but ACEi CONTRAINDICATED
  • IV magnesium sulfate to prevent seizures during labour and 24h after
  • Definitive management = deliver baby
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83
Q

PRE-ECLAMPSIA

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

A
  • Chronic HTN = HTN prior to pregnancy or <20w
  • Gestational/pregnancy induced HTN = new HTN >20w but no proteinuria + resolves after birth
  • Pre-eclampsia superimposed on chronic HTN
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84
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 but new sudden rise in proteinuria or BP
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85
Q

IUGR

What is intrauterine growth restriction (IUGR)?

A
  • Baby has not maintained its growth potential (slows or ceases)
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86
Q

IUGR

What are the two types of IUGR?

A
  • Symmetrical = entire body is proportionately small, tends to be seen with chromosomal abnormalities
  • Asymmetrical = undernourished foetus that is compensating by directing energy to maintain growth of vital organs like brain + heart
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87
Q

IUGR
What is small for gestational age (SGA)?
What can cause it?

A
  • Estimated foetal weight (EFW) or abdominal circumference (AC) below 10th centile for their gestational age
  • Constitutionally small (FHx, no pathology) or due to IUGR
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88
Q

IUGR

What is low birth weight?

A
  • Baby born with a weight <2.5kg (regardless of gestational age)
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89
Q

IUGR

What are the main causes of IUGR?

A
  • Placental insufficiency (#1) = pre-eclampsia, placenta accreta + abruption, malnutrition
  • Non-placental mediated (foetal) = genetic abnormalities (trisomy 13/18/21, Turner’s), congenital TORCH infections
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90
Q

IUGR

What are some risk factors for IUGR?

A
  • HTN
  • T2DM
  • Smoking
  • Multiple pregnancy
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91
Q

IUGR

What are some complications of IUGR?

A
  • Prematurity
  • Hypoglycaemia
  • Necrotising enterocolitis
  • Hypothermia
  • Neonatal jaundice
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92
Q

IUGR

If you were concerned about IUGR, what management would they get?

A
  • Refer for serial growth scans (every 2w to assess EFW + AC) + umbilical artery doppler (check baby getting enough blood)
  • Amniotic fluid volume may be reduced
  • MCA doppler after 32w
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93
Q

IUGR

What is the management of IUGR?

A
  • Delivery (corticosteroids if <34w) if static growth, absent end-diastolic flow on doppler or abnormal CTG
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94
Q

MACROSOMIA
What is large for gestational age?
What is macrosomia?

A
  • Estimated foetal weight above the 90th centile for their gestational age
  • Baby with a weight >4kg
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95
Q

MACROSOMIA

What are the causes of macrosomia?

A
  • Constitutionally large
  • Maternal diabetes
  • Obesity
  • Previous macrosomia
  • Overdue
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96
Q

MACROSOMIA

What are some complications of macrosomia?

A
  • Maternal = failure to progress, perineal tears, PPH

- Foetal = shoulder dystocia, neonatal hypoglycaemia, obesity

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97
Q

MACROSOMIA

What is the management of macrosomia?

A
  • OGTT to screen for diabetes
  • Regular growth scans to assess progress
  • Check amniotic fluid index to exclude polyhydramnios
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98
Q

MULTIPLE PREGNANCY
What is the difference between monozygotic and dizygotic twins?
What are some risk factors for twins?

A
  • Mono = identical, di = non-identical (1/2 zygotes)

- Previous twins, FHx, increasing maternal age, IVF

99
Q

MULTIPLE PREGNANCY

What are some complications of multiple pregnancy?

A
  • Antenatal/labour = APH, polyhydramnios, PPH

- Foetal = prematurity, twin-twin transfusion syndrome, IUGR

100
Q

MULTIPLE PREGNANCY

What is twin-twin transfusion syndrome?

A
  • Associated with monoamniotic monozygotic twins
  • Recipient gets majority of blood so is larger with polyhydramnios and donor starved of blood > anaemic
  • Severe = laser ablation of connecting vessels
101
Q

MULTIPLE PREGNANCY

What is the management of multiple pregnancies?

A
  • Steroids if <34w

- Additional scans, iron + folate

102
Q

OLIGOHYDRAMNIOS
What is oligohydramnios?
What are some complications?

A
  • Low levels of amniotic fluid, usually amniotic fluid index <5th centile
  • Pulmonary hypoplasia, muscle contractures, prematurity
103
Q

OLIGOHYDRAMNIOS

What are some causes of oligohydramnios?

A
  • Premature rupture of membranes
  • Foetal renal problems = agenesis (Potter’s syndrome)
  • IUGR
  • Post-term gestation
104
Q

OLIGOHYDRAMNIOS

What is the management of oligohydramnios?

A
  • USS to calculate AFI or maximum pool depth + monitor for IUGR
105
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
106
Q

POLYHYDRAMNIOS

What is polyhydramnios?

A
  • Abnormally large levels of amniotic fluid, usually AFI >95th centile
107
Q

POLYHYDRAMNIOS

What are the causes of polyhydramnios?

A
  • Increased foetal urination = maternal DM, TTTS, foetal anaemia
  • Insufficient removal = oesophageal or duodenal atresia, diaphragmatic hernia
108
Q

POLYHYDRAMNIOS

What are some complications of polyhydramnios?

A
  • Maternal = respiratory compromise, UTIs, c-section need

- Foetal = prematurity, malpresentation, umbilical cord prolapse

109
Q

POLYHYDRAMNIOS

What is the management of polyhydramnios?

A
  • Exclude maternal diabetes with OGTT
  • USS monitoring = AFI or maximum pool depth
  • Amnioreduction in severe cases
110
Q

RHESUS DISEASE

What is the pathophysiology of rhesus disease?

A
  • Rhesus -ve woman + rhesus +ve foetal blood = antibodies against Rh D (sensitisation) but no issues in that pregnancy as IgM cannot cross placenta
  • Subsequent = IgG crosses placenta causing haemolytic disease of newborn
111
Q

RHESUS DISEASE

What investigations would you do if you suspected rhesus disease?

A
  • Kleihauer test to check how much foetal blood > mother’s blood after sensitising event (add acid to maternal blood as foetal cells resistant)
  • All babies born to Rh-ve women have cord blood at delivery for FBC, blood group + Direct Coombs (antiglobulin) test for Ab on baby’s RBCs
112
Q

RHESUS DISEASE

What is the management of rhesus disease?

A
  • Prophylaxis crucial as sensitisation is irreversible

- IM anti-D immunoglobulin attaches to RhD antigens to avoid recognition

113
Q

RHESUS DISEASE

When is anti-D given?

A
  • 28w + 34w routinely

- Sensitising events = APH, amniocentesis/CVS, ECV

114
Q

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

A
  • Ascending bacterial infection of amniotic fluid, membranes or placenta
  • PPROM
115
Q

CHORIOAMNIONITIS

What is the clinical presentation of chorioamnionitis?

A
  • Fever, abdominal pain + offensive vaginal discharge

- Evidence of PPROM

116
Q

CHORIOAMNIONITIS

What is the management of chorioamnionitis?

A
  • Deliver foetus (corticosteroids if <34w)

- Broad spectrum IV Abx as part of sepsis six

117
Q

GESTATIONAL DIABETES

What is Gestational Diabetes Mellitus (GDM)?

A
  • Increased insulin resistance as placental production of anti-insulin hormones like human placental lactogen
118
Q

GESTATIONAL DIABETES

What are some risk factors for GDM?

A
  • BMI >30kg/m^2
  • PMH of GDM
  • FHx of DM (first-degree)
  • Asian ethnicity
  • Previous macrosomic baby
119
Q

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

A
  • OGTT
  • Anyone with previous GDM at booking + 24–28w
  • Anyone with risk factors at 24-28w
120
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
121
Q

GESTATIONAL DIABETES

What are the complications of GDM?

A
  • Foetal = macrosomia, polyhydramnios, prematurity, obesity

- Maternal = DKA, hypoglycaemia, nephropathy

122
Q

GESTATIONAL DIABETES
What is the management of GDM?
What is an alternative treatment?

A
  • Fasting glucose <7 = lifestyle changes (exercise, low glycaemic index)
  • Fasting glucose ≥7 or ≥6 and complications = start short acting insulin ± metformin
  • Glibenclamide if cannot tolerate metformin or decline insulin
123
Q

GESTATIONAL DIABETES
What is the management of GDM if the fasting glucose is <7 and they have trialled lifestyle changes but still below target?

A
  • 1–2w = add metformin

- If still not met with metformin = add insulin (short acting)

124
Q

GESTATIONAL DIABETES

What is the management of pre-existing diabetes in pregnancy?

A
  • Stop PO hypoglycaemics apart from metformin + start insulin (short-acting)
  • Folic acid 5mg/day from pre-conception to 12w
125
Q

VTE IN PREGNANCY

What are some risk factors of VTE in pregnancy?

A
  • PMHx VTE, thrombophilia = major

- BMI >30, smoking, varicose veins, immobility, age >35

126
Q

VTE IN PREGNANCY

How do you manage VTE risk antenatally?

A
  • VTE risk assessment at booking + during admissions
  • ≥4 risk factors = immediate LMWH + continue 6w postnatally
  • 3 risk factors = LMWH from 28w + continue 6w postnatally
  • TED stockings
127
Q

VTE IN PREGNANCY
What should you not prescribe in VTE?
How would you investigate VTE?

A
  • Warfarin or DOACs
  • DVT + PE = just USS doppler
  • CXR, V/Q scan is preferred in pregnancy
128
Q

OBSTETRIC CHOLESTASIS

What is obstetric cholestasis?

A
  • Intrahepatic cholestasis = reduced outflow of bile acids from liver
129
Q

OBSTETRIC CHOLESTASIS

What are some clinical features of obstetric cholestasis?

A
  • Intense pruritus of palms + soles
  • Raised bilirubin + clinically detectable jaundice in some
  • Abnormal LFTs + raised bile acids
130
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
131
Q

INFECTIONS + PREGNANCY
What does parvovirus cause in pregnancy?
What is the management?

A
  • Cross placenta > suppression of foetal erythropoiesis > foetal hydrops
  • Intrauterine blood transfusions
132
Q

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

A
  • Streptococcus agalactiae
  • # 1 cause neonatal sepsis
  • Commonly found in maternal bowel flora
133
Q

INFECTIONS + PREGNANCY

What are the risk factors of GBS?

A
  • Prematurity, prolonged ROM, previous GBS sibling, maternal pyrexia
134
Q

INFECTIONS + PREGNANCY

What is the management options for GBS in pregnancy?

A

Intrapartum IV benzylpenicillin if:
– Previous GBS pregnancy (or can test in late pregnancy with Abx if positive)
– Previous baby with GBS
– Pyrexia >38º in labour

135
Q

INFECTIONS + PREGNANCY

What are the maternal and foetal risks of Varicella zoster?

A
  • Maternal risk = 5x greater risk of pneumonitis

- Foetal varicella syndrome = skin scarring, microphthalmia, limb hypoplasia, microcephaly + learning difficulties

136
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
137
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

138
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
139
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, congenital cataracts, cerebral palsy)
  • Discuss with local health protection unit, do not offer live vaccines like MMR in pregnancy (offer postnatally)
140
Q

ANAEMIA + PREGNANCY
Why is anaemia common in pregnancy?
When is it screened for?

A
  • Hb normally falls slightly in pregnancy due to increased plasma volume diluting Hb
  • Booking and 28w
141
Q

ANAEMIA + PREGNANCY

What are the cut-off values for anaemia in pregnancy?

A

FBC

  • 1st trimester <110
  • 2nd/3rd trimester <105
  • Postpartum = <100
142
Q

ANAEMIA + PREGNANCY

What is the management of anaemia in pregnancy?

A
  • Ferrous sulfate/fumarate and continue for 3m after deficiency corrected
143
Q

ACUTE FATTY LIVER
What is acute fatty liver of pregnancy?
How does it present?
What is the management?

A
  • Rapid accumulation of fat within the hepatocytes that occurs in the third trimester of pregnancy
  • Abdo pain, N+V, jaundice, raised ALT
  • Supportive care, delivery definitive
144
Q

THYROID + PREGNANCY
What is the management of hyperthyroidism in pregnancy?
What is the management of hypothyroidism in pregnancy?

A
  • Propylthiouracil choice in 1st trimester as carbimazole causes foetal abnormalities
  • Levothyroxine safe but often needs 50% dose increase as early as first 4–6w
145
Q

EPILEPSY + PREGNANCY

What is the management of epilepsy in pregnancy?

A
  • Preconception = 5mg folic acid, aim for monotherapy = lamotrigine or carbamazepine safest
146
Q

PROM

What is prelabour rupture of membranes (PROM) and preterm prelabour rupture of membranes (PPROM)?

A
  • Rupture of amniotic sac at least 1h prior to onset of labour at >37w
  • Rupture of amniotic sac prior to onset of labour pre-term <37w
147
Q

PROM

What are some investigations for PROM?

A
  • Sterile speculum 1st for pooling of amniotic fluid
  • USS may show oligohydramnios if speculum normal
  • Test fluid for insulin-like growth factor-binding protein 1 (IGFBP-1) or placental alpha-microglobin-1 (PAMG-1)
  • CTG for foetus (tachycardia is suggestive of infection)
148
Q

PROM

What are some complications of PPROM?

A
  • Maternal = chorioamnionitis

- Foetal = prematurity, pulmonary hypoplasia

149
Q

PROM

What is the management of PPROM?

A
  • Maternal corticosteroids if foetus <34w
  • Prophylactic PO erythromycin given to prevent chorioamnionitis for 10d
  • Consider induction at 34w (trade off)
150
Q

PREMATURITY
What is the WHO definition of prematurity?
What are the causes?

A
  • Birth before 37w
  • Spontaneous = PPROM, cervical weakness, amnionitis
  • Iatrogenic = induced labour due to a complication
151
Q

PREMATURITY
What is the clinical presentation of prematurity?
What are some risk factors?

A
  • Persistent uterine activity WITH change in cervical dilatation ± effacement
  • Multiple pregnancy, IUGR, APH, polyhydramnios
152
Q

PREMATURITY

What are the investigations for prematurity?

A
  • <30w = speculum (cervical dilation + look for amniotic fluid)
  • > 30w = TV USS to measure cervical length (<15mm + contractions diagnostic > offer Mx)
  • Foetal fibronectin test = positive in premature labour
153
Q

PREMATURITY

What are the complications of prematurity?

A
  • Neonatal = NEC, RDS, intraventricular haemorrhage, retinopathy of prematurity
154
Q

PREMATURITY

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

A
  • PV progesterone gel if cervical length <25mm at 16–24w
  • Cervical cerclage if <25mm at 16–24w with previous premature birth or cervical trauma
  • Rescue cerclage at 16–27+6 if cervical dilatation without ROM
155
Q

PREMATURITY

What is the acute management of premature labour?

A
  • Senior input with foetal CTG monitoring
  • Corticosteroids if <34w to aid surfactant production + lung development
  • Tocolysis = nifedipine or oxytocin antagonist atosiban
  • IV magnesium sulfate = neuroprotection + reduce risk of cerebral palsy
  • Delayed cord clamping > increase blood volume + Hb
156
Q

STAGES OF LABOUR

What are signs of labour?

A
  • Show (shedding of mucus plug)
  • Rupture of membranes
  • Shortening + dilation of cervix
  • Regular painful contractions
157
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 (10cm)
  • Latent phase = from 0–3cm dilation. About 6h.
  • Active phase = from 3–10cm. About 12h.
158
Q

STAGES OF LABOUR

During the active phase, how quickly do you expect dilation to occur?

A
  • Primis = 0.5cm/h, multiparous = 1cm/h
159
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
160
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])

161
Q

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

A
  • APGAR score at 1, 5 + 10 minutes
  • 10–7 = normal
  • 6–4 = moderately depressed
  • <4 = severely depressed
162
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

163
Q

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

A
  • From birth of the foetus to expulsion of placenta

- Examine placenta to ensure complete as retained products > PPH or infection

164
Q

STAGES OF LABOUR
What can be used when monitoring labour?
How can they be useful?

A

Partogram is record of key maternal + foetal data –

  • FHR, contractions, maternal pulse, BP, temp
  • Drugs, IV fluids + cervical dilation noted
  • Have alert + action line > take action
165
Q

STAGES OF LABOUR
What are the 6 cardinal movements of labour?
Note the key foetal head positions too

A
  • Engagement + descent (occiput transverse)
  • Flexion
  • Internal rotation
  • Extension (crowning = occiput anterior)
  • Restitution/external rotation
  • Expulsion
166
Q

STAGES OF LABOUR

Why does internal rotation occur?

A
  • Foetus negotiating pelvic inlet which has widest diameter transverse
167
Q

STAGES OF LABOUR

Why does restitution/external rotation occur?

A
  • Negotiate pelvic outlet as widest diameter anterior/posterior
168
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
169
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 ≥8 = favourable cervix ready for labour or induction
170
Q

FAILURE TO PROGRESS

What are the components of the Bishop score?

A
  • Cervical dilation – <1cm (0), >5cm (3)
  • Cervical consistency – firm (0), intermediate (1), soft (2)
  • Cervical effacement –<30% (0), 80% (3)
  • Cervical position – posterior (0), intermediate (1), anterior (2)
  • Foetal station – –3 (0), ≥1 (3)
171
Q

FAILURE TO PROGRESS

What are some methods of inducing labour?

A
  • Membrane sweep (often 40/41w antenatal visit)
  • Vaginal prostaglandin E2 (PGE2) pessary to ripen cervix
  • Maternal oxytocin infusion to stimulate contractions
  • Amniotomy
  • Cervical ripening balloon
172
Q

FAILURE TO PROGRESS
What is a complication of labour induction?
What is the management?

A
  • Uterine hyperstimulation = frequent uterine contractions

- Remove vaginal PGE2/stop oxytocin infusion, tocolytic terbutaline

173
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)
174
Q

FAILURE TO PROGRESS
How can ‘power’ cause failure to progress?
Who is it common in?

A
  • Poor uterine contractions

- Common in primigravida women

175
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 = common in developing countries

176
Q

FAILURE TO PROGRESS

How can ‘passenger’ cause failure to progress?

A
  • Size = macrosomia, size of head
  • Attitude = posture of foetus
  • Lie = longitudinal, transverse, oblique
  • Presentation = part closest to cervix
177
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

- May need episiotomy, instrumental delivery or c-section

178
Q

FAILURE TO PROGRESS
How is failure to progress in the third stage of labour defined?
How would you manage this?
What is a potential risk?

A
  • Delay = >30m if active Mx or >60m with physiological
  • Oxytocin to cause uterus contraction + expel placenta
  • Cord clamp + careful cord traction to guide placenta out (excessive force > snapped cord or uterine inversion)
179
Q

BREECH

What are the types of breech presentation?

A
  • Extended (Frank) = #1 = hips flexed, knees extended, buttocks presenting
  • Flexed (Complete) = hips + knees flexed so buttocks + feet presenting (cannonballing)
  • Footling = one/both feet come first with buttocks higher
180
Q

BREECH
What complication is more common in breech presentations?
What are some risk factors of breech?

A
  • Cord prolapse

- Fibroids, placenta praevia, poly/oligohydramnios, prematurity

181
Q

BREECH

What are the investigations for breech?

A
  • Abdominal exam = longitudinal lie, head palpated at fundus

- Dx on antenatal USS, <36w = not important unless woman in labour

182
Q

BREECH

What is the management of breech?

A
  • External cephalic version (ECV) = 36w nulliparous or 37w multiparous
  • C-section if ECV is unsuccessful or contraindicated
183
Q

BREECH

What are some contraindications for ECV?

A
  • APH within 7d
  • Multiple pregnancies
  • Abnormal CTG
184
Q

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

A
  • Long axis of foetus relative to longitudinal axis of uterus
  • Longitudinal, transverse, oblique, unstable (actively changing)
185
Q

FOETAL LIE

What are some risk factors for foetal lie?

A
  • Multiple pregnancy
  • Polyhydramnios
  • Fibroids
186
Q

FOETAL LIE

What are some investigations for foetal lie?

A
  • Abdo exam = neither head nor buttocks presenting

- USS can be used to confirm lie, often antenatally

187
Q

FOETAL LIE

What are some complications of abnormal lie?

A
  • PROM

- Cord prolapse (highest risk in transverse lie)

188
Q

FOETAL LIE

What is the management for foetal lie?

A
  • <36w = none as most will spontnaeously > longitudinal

- >36w = ECV even in early labour if membranes intact or c-section

189
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
190
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
191
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
192
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
193
Q

CTG
What are accelerations?
What do they show you?

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

- Reassuring as baby moving

194
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)
195
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

196
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

197
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

198
Q

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

A
  • Umbilical cord descends ahead of presenting part of foetus which can lead to compression of cord or cord spasm > foetal hypoxia + morbidity or mortality
199
Q

CORD PROLAPSE

What are some risk factors for cord prolapse?

A
  • Prematurity
  • Polyhydramnios
  • Multiple pregnancy
200
Q

CORD PROLAPSE

What are the investigations for cord prolapse?

A
  • Diagnosis on vaginal exam = cord at introitus or palpable vaginally
  • Foetal CTG distress (heart decelerations + bradycardia)
201
Q

CORD PROLAPSE

What is the management of cord prolapse?

A
  • 999/emergency buzzer, senior team
  • Delivery = c-section (can trial instrumental if cervix dilated)
  • Knees to chest position
  • Push presenting part back into uterus to prevent compression
  • Fill bladder with 500ml warmed saline
  • Avoid exposure + cord handling as can cause spasm
  • Tocolytics to abolish contractions
202
Q

SHOULDER DYSTOCIA
What is shoulder dystocia?
What are some risk factors?

A
  • Failure of anterior shoulder to pass under the pubic symphysis after delivery of foetal head
  • Foetal macrosomia, DM, high maternal BMI
203
Q

SHOULDER DYSTOCIA

What are some complications of shoulder dystocia?

A
  • Maternal = PPH, perineal tears

- Neonatal = hypoxia, brachial plexus injury, cerebral palsy, death

204
Q

SHOULDER DYSTOCIA

What is the management of shoulder dystocia?

A

HELPERR –

  • Help (emergency buzzer, seniors)
  • Evaluate for episiotomy (enlarge opening)
  • Legs = McRobert’s
  • Pressure = suprapubic
  • Enter = pelvis for rotation = Rubin II, woods’ screw + reverse woods’ screw
  • Remove = posterior arm
  • Replace = head in vagina + deliver by c-section (Zavanelli)
205
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

206
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
207
Q

INSTRUMENTAL DELIVERY

What are the main risks of ventouse delivery?

A
  • Cephalohaematoma = collection of blood between periosteum + skull, does not cross suture lines, presents hours after
  • Caput Succedaneum = Crosses Sutures, diffuse oedema outside periosteum, resolve in few days, conehead present at birth
208
Q

PAIN RELIEF

What are some non-pharmacological pain relief for labour?

A
  • Hypnotherapy
  • Water birth
  • Controlled breathing
  • TENS
209
Q

PAIN RELIEF

What simple analgesia can be used in labour?

A
  • Paracetamol + codeine useful in early labour

- Avoid NSAIDs

210
Q

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

A
  • Gas + air (nitrous oxide + O2 50/50 mixed)
  • Rapid onset, self-limiting
  • N+V, dizziness
211
Q

PAIN RELIEF

What opioids can be used for pain relief?

A
  • Single shot IM opioids (diamorphine, pethidine > avoid in patients with epilepsy as can cause seizures)
212
Q

PAIN RELIEF
What more invasive management may be offered?
What are some adverse effects?

A
  • Epidural or spinal with bupivacaine

- Post-dural puncture headache, prolonged 2nd stage, increased probability of instrumental delivery

213
Q

PERINEAL TEARS

What are some risk factors for perineal tears?

A
  • Macrosomia
  • Shoulder dystocia
  • Forceps
214
Q

PERINEAL TEARS
What is a first degree perineal tear?
How is it managed?

A
  • Injury to superficial skin, no muscle involvement

- Do NOT require repair

215
Q

PERINEAL TEARS
What is a second degree perineal tear?
How is it managed?

A
  • Injury to perineal muscle but NOT anal sphincter

- Suturing on ward by experienced midwife or clinician

216
Q

PERINEAL TEARS
What is a third degree perineal tear?
How is it managed?

A
  • Injury involving anal sphincter complex (3A <50% EAS, 3B >50% EAS, 3C IAS torn)
  • Repair in theatre by clinician
217
Q

PERINEAL TEARS
What is a fourth degree perineal tear?
How is it managed?

A
  • Injury to perineum, anal sphincter complex AND rectal mucosa
  • Repair in theatre by clinican
218
Q

PROLONGED PREGNANCY
What is a prolonged pregnancy?
What are the complications with this?

A
  • Pregnancy exceeding 42w from LMP

- Macrosomia, oligohydramnios, reduced placental perfusion, meconium aspiration syndrome > severe pneumonitis

219
Q

UTERINE RUPTURE
What is a uterine rupture?
What are some risk factors?

A
  • Complication of labour where myometrium bursts

- VBAC, previous uterine surgery, increased BMI, oxytocin

220
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
221
Q

UTERINE RUPTURE

What is the management of uterine rupture?

A
  • ABCDE and emergency c-section
222
Q

AMNIOTIC EMBOLISM
What is an amniotic fluid embolism?
What are some risk factors?

A
  • Amniotic fluid/foetal cells enter mother’s blood stream causing an immune reaction
  • Increasing maternal age + induction of labour
223
Q

AMNIOTIC EMBOLISM

What is the clinical presentation of amniotic fluid embolism?

A
  • During labour or immediate postpartum
  • Symptoms = SOB, sweating, anxiety
  • Signs = hypoxia, shock, arrhythmia + MI
224
Q

AMNIOTIC EMBOLISM

What is the management of amniotic fluid embolism?

A
  • ABCDE approach

- Critical care management often supportive

225
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 EBL
- Major = >1000ml, clinically in shock
Secondary = excessive blood loss from genital tract between 24h–12w after delivery

226
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

227
Q

PPH

What are the before birth and during labour risk factors for PPH?

A
  • Before birth = APH, previous PPH, multiple pregnancy

- Labour = c-section, perineal tear, macrosomia

228
Q

PPH

How might uterine atony present in PPH?

A
  • Unpalpable uterus on abdo exam (should normally be palpable in period following birth)
229
Q

PPH

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

A
  • Empty bladder as full bladder reduces uterine contractions
  • Active Mx of third stage (oxytocin)
  • IV TXA during c-section in third stage of labour if high risk
230
Q

PPH

What is the initial acute management of PPH?

A
  • ABCDE resus = 2x large bore cannulas, X match, major haemorrhage protocol, IV fluids
  • Mechanically massage uterus through abdomen
231
Q

PPH

What is the medical management of PPH?

A
  • IV syntocinon or IV ergometrine (can combine as syntometrine) but ergometrine C/I in HTN as vasoconstrictor
  • IM carboprost (prostaglandin analogue = caution in asthma)
  • Sublingual misoprostol (prostaglandin analogue)
232
Q

PPH

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

A
  • Intrauterine balloon tamponade (1st line in uterine atony)
  • Other surgical = B-lynch sutures, ligation of uterine or internal iliac arteries
  • Hysterectomy as last resort (may save life)
233
Q 
PUERPERAL PYREXIA
What is puerperal pyrexia?
What are the causes?
What is the presentation of the most common cause?
What is the management
A
  • Temp >38 in first 14d postpartum
  • Endometritis #1, UTI, mastitis, VTE
  • Foul smelling discharge, heavy bleeding, abdo pain
  • Endometritis = hospital for IV Abx (clindamycin/gent)
234
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

235
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
236
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

237
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

238
Q

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

A
  • All babies screened within 4w of birth ideally (up to 3m)
  • Otoacoustic emission test
  • If above abnormal = auditory brainstem response test
239
Q

MENTAL HEALTH
What are baby blues?
What is the management?

A
  • Brief period of tearfulness, anxiety + emotional lability, 3–7d after birth
  • Reassurance + health visitor surveillance
240
Q

MENTAL HEALTH
What is postnatal depression?
How can it be screened for?

A
  • Depressive episode, temporally related to childbirth, often within 1m
  • Edinburgh postnatal depression scale
241
Q

MENTAL HEALTH

What is the management of postnatal depression?

A
  • CBT

- SSRIs sertraline or paroxetine ok in breastfeeding

242
Q

MENTAL HEALTH
What is postpartum/puerperal psychosis?
What is the management?

A
  • Acute psychotic episode often 2–3w postpartum

- Manage with admission to hospital, ideally Mother and Baby unit

243
Q

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

A
  • Pituitary necrosis secondary to a PPH

- Replacement of deficient hormones

244
Q

SHEEHAN’S SYNDROME

How does Sheehan’s syndrome present?

A
  • Low ACTH = adrenal insufficiency
  • Low LH + FSH = amenorrhoea, infertility, loss of libido
  • Low TSH = hypothyroidism
  • Low prolactin = reduced lactation

FINALS (20 decks)

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