GOSH Flashcards

Study cards for GOSH

1
Q

What are the six first stages of foetal development?

A
  1. OVULATION- On day 14 this is caused by the release of LH
  2. FERTILIZATION- this occurs in the fallopian tube
  3. CELL DIVISION- cells divide into zygote/morula/blastocyst
  4. TRANSPORT- the blastocyst is transported to the uterine cavity.
  5. IMPLANTATION- On day 23 the blastocyst is implanted into he decide in the funds of the uterus.
  6. B-hCG PRODUCTION- after implantation B-hCG is produced which causes the ovary to produce progesterone from the corpus lute until 10-12 weeks, where the placenta takes over.
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2
Q

How do hCG levels function?

A

They rise rapidly up to 10 weeks but drop after 14 weeks

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3
Q

When is hCG detected in pregnancy?

A

it is the basis of a pregnancy test and can be detected in serum and urine 4 weeks after LMP

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4
Q

What value of hCG is a positive result?

A

> 25IU/ml

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5
Q

How is progesterone activated in pregnancy?

A

it is stimulated by hCG

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6
Q

What symptoms of pregnancy can result due to progesterone?

A
  • Stress incontinence
  • Acid reflux
  • Constipation
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7
Q

How does progesterone trigger certain symptoms in pregnancy?

A

By inducing smooth muscle relaxation

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8
Q

How is pregnancy diagnosed?

A

CLINICALLY- using signs and symptoms
EXAMINATION
INVESTIGATIONS- hCG and USS

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9
Q

What are the main signs and symptoms of pregnancy?

A
  • Amenorrhea
  • Nausea and vomiting
  • Frequency of micturition
  • Excessive lethargy or fatigue
  • Breast tenderness or heaviness
  • Foetal movements or quickening
  • Abnormal cravings
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10
Q

What can be seen on clinical examination of ?pregnancy

A
  • the vagina and cervix have a bluish tinge due to blood congestion
  • the size of the uterus may be estimated by bimanual examination
  • after 12 weeks the uterus is palpable abdominally and the foetal heart may be head using a hand-held Doppler
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11
Q

What can be seen on ultrasound at 4-5 weeks?

A

Gestation sac

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12
Q

What can be seen on ultrasound at 5-6 weeks?

A

Yolk sac

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13
Q

What can be seen on ultrasound at 6 weeks?

A

Foetal pole

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14
Q

What can be seen on ultrasound at 6-7 weeks?

A

Foetal heart activity

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15
Q

What can be seen on ultrasound at 8 weeks?

A

Limb buds and foetal movement

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16
Q

What are the landmarks of pregnancy before 12 weeks?

A
  • Organs develop
  • Placenta assumes major role (gas exchange, nutrient/waste transfer, steroidogenesis)
  • Placenta takes over estrogen 10-12 weeks
  • Highest risk of miscarriage
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17
Q

What are the landmarks of pregnancy after 12 weeks?

A

Growth and maturation

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18
Q

What are the intrinsic maternal factors governing foetal growth?

A
  • Height
  • Weight
  • Parity (number of previous pregnancies)
  • Ethnic group
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19
Q

What are the intrinsic foetal factors governing growth?

A
  • Sex

- Genes/inherited conditions

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20
Q

What are the extrinsic maternal factors governing foetal growth?

A
  • Social class
  • Nutritional status
  • Environment: altitude
  • Pre-existing disease (cardiac/renal/resp/vasc)
  • Pregnancy related disease (HTN, diabetes)
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21
Q

What are the extrinsic foetal factors governing growth?

A
  • Nutrition (from the placenta)
  • Teratogenic (tobacco, narcotics, alcohol, medication)
  • Infective (viral, protozoan, others (listeria, syphilis)
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22
Q

What are the main components of a prenatal assessment history?

A
  1. PMH
  2. POH (past obstetric history- small babies before?)
  3. DH
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23
Q

What are the landmarks for fundal height?

A
  • At 13-14 weeks the top of the uterus is usually at the mother’s pubic bone.
  • At 20-22 weeks the top of the uterus is usually at the mother’s umbilicus
  • At 36-40 weeks, the top of the uterus is almost at the bottom of the mother’s ribs
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24
Q

What are the components of BPP (biophysical profile)?

A
  • foetal breathing movements
  • foetal movements
  • foetal tone
  • amniotic fluid volume
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25
Q

What are the blood flow characteristics from foetus to placenta?

A

umbilical

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26
Q

What are the blood flow characteristics from the mother to placenta?

A

uterine

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27
Q

How is EDD calculated?

A

LMP + 7/7 + 12/12 ( - 3/12)

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28
Q

Which are the first set of antenatal bloods taken?

A
  • FBC
  • Group and save
  • Haemoglobinopathies
  • Blood group and antibody screen (for rhesus)
  • HIV
  • Hepatitis B
  • Syphilis
  • Rubella
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29
Q

What is important to advise during the first antenatal appointment?

A
  • Flu vaccine
  • Folic acid
  • Vitamin D
  • Smoking cessation
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30
Q

In rhesus isoimmunisation, which gene is must commonly the cause?

A

D gene

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31
Q

What is the recommended dose of folic acid?

A

400 micrograms/day

In mothers with higher risk- 5mg/day

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32
Q

What are the main principles of antenatal appointments?

A
  • General maternal well-being
  • Blood pressure
  • Urinalysis
  • Foetal movements
  • Foetal heart rate
  • Fundal height- symphysis pubis
  • Measure plot symphysis- fundal height
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33
Q

What are the potential sensitizing events for rhesus isoimmunisation?

A
  • termination of pregnancy
  • ectopic pregnancy
  • vaginal bleeding >12 weeks
  • external cephalic version
  • blunt abdominal trauma
  • invasive uterine procedure (amniocentesis)
  • intrauterine death
  • delivery
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34
Q

How does rhesus prophylaxis occur?

A

if sufficient anti-D immunoglobulin is given to the mother it will bind to any foetal red cells in her circulation carrying the D antigen.
This prevents her own immune system from recognizing them and becoming sensitized.

Anti-D (500IU) is given to all women who are rhesus negative) WEEK 28

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35
Q

What are the four components routinely screened for in booking?

A
  1. Rhesus negative
  2. Haemoglobinopathies
  3. Foetal anomalies
  4. Infectious diseases
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36
Q

Which four infectious diseases are routinely screened for?

A
  1. HIV
  2. Hepatitis B
  3. Syphilis
  4. Rubella
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37
Q

What is NOT routinely screened for?

A
  • Hepatitis C
  • Chlamydia
  • Group B Strep
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38
Q

What is entailed in ‘combined screening’ for Downs’ Syndrome?

A
  • Nuchal translucency scan (thickened)
  • Maternal blood test for hCG (high)
  • Maternal blood test for PAPPA (low)(pregnancy associated plasma protein A)
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39
Q

What is offered to mothers considered as ‘high risk’ for Down’s Syndrome fetuses?

A
  • CVS (chorionic villus sampling) from 11 weeks

- Amniocentesis from 15 weeks

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40
Q

When is ‘combined screening’ in Down’s Syndrome performed?

A

In the first trimester from 11+2 to 14+2

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41
Q

What is the ‘quadruple test’ in Down’s syndrome screening?

A

Maternal blood test for

  1. AFP (alpha feto-protein) (LOW)
  2. hCG (HIGH)
  3. Estriol (LOW)
  4. Inhibin-A
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42
Q

When is the ‘quadruple test’ performed?

A

15-20 weeks

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43
Q

What test is available in the private sector?

A

NIPT (non-invasive prenatal test)

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44
Q

When is the foetal anomaly/anatomy scan done?

A

From 18+0 week until 20+6

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45
Q

What are the indications for CVS (chorionic villous sampling)?

A
  • for karyotyping if 1st trimester screening test suggests high risk for aneuploidy
  • for DNA analysis if parents are carriers of an identifiable gene mutation such as cystic fibrosis or thalassaemia
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46
Q

What are the benefits of CVS (chorionic villous sampling)?

A
  • Allows 1st trimester termination of pregnancy if an abnormality is detected (which can be done surgically and before the pregnancy has become physically apparent)
  • Rapid karyotyping as trophoblast cells are more easily cultured than by amniocentesis
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47
Q

What are the risks of CVS (chorionic villous sampling)?

A
  • Miscarriage as a result of CVS is estimated at 1%
  • Increased risk of vertical transmission of blood-borne viruses such as HIV and hep B
  • False negative results (rare) from contamination with maternal cells
  • Placental mosaicism producing misleading results
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48
Q

What are the indications for amniocentesis?

A
  • For karyotyping if screening tests suggests aneuploidy.
  • For DNA analysis if parents are carriers of an identifiable gene mutation such as cystic fibrosis or thalassemia.
  • For enzyme assays looking for inborn errors of metabolism.
  • For diagnosis of foetal infections such as CMV and toxoplasmosis
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49
Q

What are the benefits for amniocentesis?

A
  • Lower procedure attributed miscarriage rate than CVS.

- Less risk of maternal contamination or placental mosaicism

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50
Q

What are the risks for amniocentesis?

A
  • Miscarriage estimated at 1%- but this risk is only a little higher than the natural risk.
  • Failure to culture cells
  • Full karyotyping may take 3 weeks (results for certain chromosomal abnormalities may be available more rapidly using FISH or PCR).
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51
Q

Gynaecological purposes of USS

A
  • Assessment of pelvic mass and normal pelvic anatomy
  • Follicle tracking in ovulation induction
  • Endometrial cavity assessment in abnormal menstrual bleeding or sub-fertility.
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52
Q

First trimester indications for USS

A
  • Exclusion of ectopic pregnancy
  • Assessment of pregnancy viability
  • Estimation of gestational age
  • Detection of multiple pregnancy
  • Diagnosis of structural abnormalities
  • Screening for chromosomal abnormalities
  • Determination of chronicity
  • Detection of retained products of conception post miscarriage
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53
Q

Second trimester indications for USS

A
  • Diagnosis of structural abnormalities
  • Screening for chromosomal abnormalities
  • Doppler for foetal assessment
  • Assessment of uterine arteries
  • Help other diagnostic or therapeutic techniques
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54
Q

Third trimester indications for USS

A
  • Assessment for foetal growth
  • BPP for foetal wellbeing
  • Diagnosis of placenta praevia
  • Determining presentation in difficult cases
  • Doppler for foetal assessment
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55
Q

What are the benefits of USS

A
  • Aids diagnosis in gynaecology
  • Maternal reassurance
  • Screening for and detection of abnormalities
  • Reduction of perinatal mortality in high-risk pregnancy
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56
Q

What are some of the risks associated with substance abuse in pregnancy?

A
  1. Preterm birth and pre-maturity
  2. IUGR
  3. Low birth weight
  4. Symptoms of drug withdrawal
  5. Increased stillbirth (placental abruption)
  6. Neonatal mortality (babies can ‘withdraw’)
  7. SIDS (Sudden Infant Death Syndrome)
  8. Physical and neurological damage from drugs/ violence
  9. Foetal alcohol syndrome
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57
Q

What help is available for smoking cessation in pregnancy?

A
  • Help from specialist smoking cessation advisers

- Nicotine replacement therapy (patches or gum) may be used in pregnancy

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58
Q

Which foods should be avoided in pregnancy?

A
  • Some cheeses (potential listeria)
  • Raw or partly cooked eggs (salmonella)
  • Caffeine (link to miscarriage)
  • Vitamins/ fish oil supplements
  • Peanuts
  • Milk/yoghurt
  • Ice cream
  • Foods with soil on them
  • Herbal teas
  • Game
  • Pâté
  • Raw or undercooked meat (e. coli)
  • Liver (e.coli)
  • Cold cured meat (e. coli)
  • Fish (risk of mercury)
  • Raw shellfish (vibrio)
  • Smoked fish
  • Sushi (salmonella)
  • Liquorice
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59
Q

Management of backache and sciatica in pregnancy

A
  1. lifestyle modification (sleeping positions)
  2. alternative therapies (relaxation and massage)
  3. physiotherapy input (e.g. back care classes)
  4. simple analgesia
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60
Q

Management of symphysis pubic dysfunction in pregnancy

A
  1. physiotherapy advice and support
  2. simple analgesia
  3. limit abduction of legs at delivery
  4. Caesarean section is not indicated
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61
Q

Management of hemorrhoids in pregnancy

A
  1. Avoid constipation from early pregnancy
  2. Ice packs and digital reduction of prolapsed hemorrhoids
  3. Suppositories and topical agents for symptomatic relief
  4. If thromboses, may require surgical referral
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62
Q

Management of constipation in pregnancy

A
  1. lifestyle modification (increasing fruit, fibre and water intake)
  2. fibre supplements
  3. osmotic laxatives (lactuloses)
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63
Q

Management of varicose veins in pregnancy

A
  1. regular exercise
  2. compression hosiery
  3. consider thromboprophylaxis if other risk factors are present
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64
Q

Management of carpel tunnel syndrome in pregnancy

A
  1. Sleeping with hands over the side of the bed
  2. Wrist splints
  3. If evidence of neurological deficit, surgical referral may be indicated.
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65
Q

Management of GOR in pregnancy

A
  1. lifestyle modification (e.g. sleeping propped up, avoiding spicy food)
  2. Alignate preparations and simple antacids
  3. If severe, H2 receptor antagonists (ranitidine)
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66
Q

Management of nausea and vomiting (morning sickness) in pregnancy

A
  1. lifestyle modification (eating small meals, increasing fluid intake)
  2. ginger (teas, etc)
  3. acupressure
  4. antiemetics (prochlorperazine, promethazine, metoclopramide)
  5. May warrant hospital admission if severe (hyperemesis gravidarum)
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67
Q

What is hyperemesis gravidarum?

A

Excessive vomiting in pregnancy

Patients with multiple or molar pregnancies are at increased risk, due to high levels of hCG.

The individual is unable to maintain adequate hydration and endangers fluid, electrolyte and nutritional status.

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68
Q

When is the peak onset for hyperemesis gravidarum?

A

6-11 weeks

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69
Q

What are the signs and symptoms associated with hyperemesis gravidarum?

A
  • vomiting
  • weight loss
  • muscle wasting
  • dehydration
  • liver tenderness
  • ptyalism (inability to swallow saliva)
  • hypovolemia
  • electrolyte imbalance: ketones, behavior disorders
  • hematemesis (Mallory-Weiss tears)
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70
Q

What are the maternal complications associated with hyperemesis gravidarum?

A

liver and renal failure

hyponatraemia and rapid reversal of hyponatraemia leading to central portion myelinosis

Thiamine deficiency may lead to Wernicke’s encephalopathy

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71
Q

What are the fetal complications associated with hyperemesis gravidarum?

A

IUGR

Foetal death in cases with Wernicke’s encephalopathy.

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72
Q

What is the conservative management for hyperemesis gravidarum?

A
  1. Exclude other causes e.g. urine infection, thyrotoxicosis
  2. Reassurance and simple advice: small frequent amounts of fluid and little amounts of carbs
  3. Admit if not tolerating oral fluid
  4. Accupuncture and complimentary therapies
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73
Q

Antiemetic doses for hyperemesis gravidarum.

A

Metoclopramide 10mg/8h PO/IM/IV
Cyclizine 50mg/8h
Prochlorperazine 12.5mg IM/IV tds
Prochlorperazine 5mg PO tds

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74
Q

Investigations for hyperemesis gravidarum

A

URINALYSIS- to detect ketones in urine
MSU- to exclude UTIs
U&Es- decreased K+, decreased Na+, metabolic hypchloraemic alkalosis)
LFTs- (increased transaminases, decreased albumin)
USS- to exclude multiple and molar pregnancies and confirm

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75
Q

What is the medical management for hyperemesis gravidarum?

A
  1. IV fluids (NaCl/ Hartmann’s (avoid dextrose as this can precipitate WE))
  2. Daily U&Es- replace potassium if necessary
  3. Keep NBM for 24 hours, then introduce light diet as tolerated
  4. Antiemetics if no response to IV fluid and electrolyte replacement alone.
  5. Vitamin supplementation- especially in the B complex e.g. thiamine
  6. Corticosteroid if vomiting is protracted and unresponsive to fluids and antiemetics
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76
Q

Thiamine doses for hyperemesis gravidarum

A

thiamine hydrochloride 25-50mg PO tds
OR
thiamine 100mg IV infusion weekly

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77
Q

Corticosteroid doses for hyperemesis gravidarum

A

Prednisolone 40-50mg PO daily in divided doses
OR
Hydrocortisone 100mg/12h IV

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78
Q

What are the measurements used to assess foetal size?

A

BPD- biparietal diameter (used in 14-20 wks)
HC- head circumference
AC- abdominal circumference (most important)
FL- femur length

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79
Q

Why a uterus would measure as small for dates

A
  • Wrong dates
  • Oligohyramnios (deficiency of amniotic fluid)
  • IUGR
  • Presenting part deep in the pelvis
  • Abnormal lie of foetus
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80
Q

Why a uterus would measure as large for dates

A
  • Wrong dates
  • Polyhydramnios (excessive amniotic fluid)
  • Macrosomia
  • Multiple pregnancy
  • Presence of fibroids
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81
Q

Causes of polyhydramnios

A
  • Idiopathic
  • Maternal disorders (diabetes, renal failure)
  • Twins
  • Foetal anomaly (e.g. gastro obstructions or inability to swallow, chest abnormalities, myotonic dystrophy)
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82
Q

Clinical features of polyhydramnios

A
  • Maternal discomfort
  • Large for dates
  • Foetal parts difficult to palpate
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83
Q

What are the complications of polyhydramnios?

A
  • Preterm labour
  • Maternal discomfort
  • Abnormal lie and malrepresentation
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84
Q

Management for polyhydramnios

A

To diagnose foetal anomaly: detailed ultrasound screening

To diagnose diabetes: maternal blood glucose testing

To reduce liquor: If <34 weeks and severe, amnioreduction or use of NSAIDS to reduce foetal urine output

Consider steroids if <34 weeks

Delivery should be vaginal unless persistent unstable lie or other obstetric indication

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85
Q

Factors of foetal movement

A
  1. Most movements begin 18-20 weeks
  2. Usually kick, flutters, swishes or rolls
  3. Afternoon and evenings are peak activity
  4. Sleep usually occurs between 20 and 40 mins
  5. Movements increase until 32 weeks and then stabilize.
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86
Q

How to assess foetal movement

A

Lie down on the left side and focus on baby’s movements for 2 hours
If fewer than 10 separate movements during 2 hours, take action

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87
Q

Reasons for decreased movements

A
  • Placenta is at the front of the uterus it can reduce ability to feel baby movements
  • If the baby’s back is lying at the front of the uterus, one may feel fewer movements
  • Drugs such as strong pain relief or sedatives
  • Alcohol and smoking
  • Foetal illness/distress
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88
Q

How is prolonged pregnancy defined

A

Pregnancy that exceeds 42 weeks (294 days) from the first day of the LMP

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89
Q

What are maternal complications of prolonged pregnancy?

A
  • Maternal anxiety and psychological morbidity

- Increased intervention (induction of labour, operative delivery with increased risk of genital tract trauma)

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90
Q

What are the foetal complications of prolonged pregnancy?

A
  • Perinatal mortality increases after 42 weeks of gestation
  • Intrapartum deaths are 4x more common
  • Early neonatal deaths are 3x more common
  • Meconium aspiration and assisted ventilation
  • Oligohydramnios
  • Macrosomia, shoulder dystocia and foetal injury
  • Cephalhaematoma
  • Foetal distress in labour
  • Neonatal- hypothermia, hypoglycemia, polycythemia and growth restriction
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91
Q

Management of prolonged pregnancy

A
  • Confirm the EDD is accurately as possible
  • Assess any other risk factors which may be an indication to induce close to the EDD
  • Offer stretch and sweep at 41 weeks
  • Offer induction of labour between 41 and 42 weeks
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92
Q

Fetal monitoring during prolonged pregnancy

A
  • Initial USS assessment of growth and amniotic fluid volume
  • Daily CTGs (cardiotocography- foetal heart monitoring)
  • Report any decrease in foetal movements
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93
Q

PPROM

A

Preterm Pre-labour Rupture of Membranes

  • this is when the amniotic sac ruptures before 37 weeks.
  • this complicates 1/3 of preterm deliveries and is associated with 1/3 of overt infections
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94
Q

What are the signs and symptoms of chorioamnionitis?

A
  • Fever/ malaise
  • Abdominal pain, including contractions
  • Purulent/ offensive vaginal discharge
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95
Q

What is seen on examination in chorioamnionitis?

A
  • Maternal pyrexia
  • Tachycardia
  • Uterine tenderness
  • Foetal tachycardia
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96
Q

What is seen on speculum examination in chorioamnionitis?

A
  • Offensive vaginal discharge (yellow/ brown)
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97
Q

What investigations are used in PPROM?

A
  • Speculum examination
  • FBC
  • CRP (raised WCC and CRP indicate infection)
  • Swabs (high and low vaginal swabs)
  • MSU
  • CTG (cardiotocography)
  • USS for foetal presentation, EFW (estimated foetal weight) and liquor volume
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98
Q

Management of PPROM with evidence of chorioamnionitis

A
  • Steroids (dexamethasone or betamethasone 12mg IM)
  • Deliver the baby
  • Broad spectrum antibiotic cover (erythromycin 250mg QDS for 10 days)
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99
Q

Conservative management of PPROM with no evidence of chorioamnionitis

A
  • Admit to hospital
  • Inform SCBU (special care baby unit) and liaise with neonatologists
  • Discharge after 48 hours and review in day unit twice a week for bloods and vital obs.
  • Induction after 34 weeks
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100
Q

Medical management of PPROM with no evidence of chorioamnionitis

A
  • Steroids (12mg betamethasone IM two doses 24 hours apart)

- Prophylactic antibiotics (erythromycin 250mg QDS for 10 days)

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101
Q

What is the prognosis for gestation at PPROM?

A

PPROM at <20 weeks- few survivors

PPROM >22 weeks- survival goes up to 50%

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102
Q

What is classified as a high risk pregnancy?

A

One in which the probability of an adverse outcome in the mother and/or baby is greater than that for an average pregnant woman

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103
Q

What are some maternal conditions for a high risk pregnancy?

A
  • Obesity
  • Diabetes
  • HTN
  • Chronic disease (CKD, SLE, respiratory disease)
  • Infection
  • Previous surgery
  • VTE (4x risk if family history of estrogen related VTE)
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104
Q

What are some social factors associated with high risk pregnancy?

A
  • Teenage pregnancy
  • Maternal age >35
  • High parity (>4 PPH) and low interpregnancy interval
  • Poor socioeconomic conditions
  • Alcohol intake
  • Substance abuse
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105
Q

What obstetric issues arise in high risk pregnancies?

A
  1. Caesarean section
  2. Preterm delivery
  3. Recurrent miscarriage (3+)
  4. Stillbirth
  5. Pre-eclampsia
  6. Gestational diabetes
  7. Third degree tear
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106
Q

What problems can arise during labour of a high risk pregnancy?

A
  1. Meconium stained liquor
  2. Blood stained liquor
  3. Worrying CTG (cardiotocography)
  4. Need for oxytocin infusion
  5. Lack of progress
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107
Q

What are the main principles of monitoring high risk pregnancy?

A
  • Counselling (mode of delivery)
  • Symphysis- fundal height
  • Extra investigations (GTT- glucose tolerance test, BP)
  • Routine monitoring of foetal movement
  • Ultrasound assessment of foetal growth
  • Uterine artery doppler
  • CTG (cardiotocography)
  • Anaesthetic review
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108
Q

What is IUGR (FGR)?

A

Intra-uterine Growth Restriction which implies that a fetus is pathologically small.

Also known as foetal growth restriction

It is analogous to ‘failure to thrive’

SGA can be used as a surrogate marker where if the estimated weight of the fetus is below the 10th percentile for its gestational age.

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109
Q

Important risks of IUGR (FGR)

A
  • Perinatal mortality is 6-10x greater
  • Incidence of cerebral palsy is 4x greater
  • 30% of all stillborn infants are growth restricted
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110
Q

What are some potential complications of IUGR (FGR)

A
  • Intrapartum fetal distress and asphyxia
  • Meconium aspiration
  • Emergency C section
  • Necrotizing enterocolitis
  • Hypoglycaemia and hypocalcemia
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111
Q

What are the maternal causes of IUGR (FGR)?

A
  1. CHRONIC MATERNAL DISEASE- HTN, cardiac disease, chronic renal failure
  2. SUBSTANCE ABUSE- alcohol, recreational drug use, smoking
  3. AUTOIMMUNE DISEASES- antiphospholipid antibody syndrome
  4. GENETIC DISORDERS- Phenylketonuria
  5. POOR NUTRITION
  6. LOW SOCIOECONOMIC STATUS
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112
Q

What are the placental causes of IUGR (FGR)?

A
  1. ABNORMAL TROPHOBLAST INVASION- preeclampsia, placental accreta
  2. ABNORMAL UMBILICAL CORD OR CORD INSERTION
  3. ABRUPTION
  4. PLACENTAL LOCATION- placenta praaevia
  5. TUMOURS: chorioangiomas (placental haemangiomas)
  6. INFARCTION
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113
Q

What are the foetal causes of IUGR (FGR)?

A
  1. GENETIC ABNORMALITIES- trisomy 13. 18/21, Turner’s syndrome, triploidy
  2. CONGENITAL ABNORMALITIES- cardiac (tetralogy of Fallot, transposition of the great vessels, gastroschisis.
  3. MULTIPLE PREGNANCY
  4. CONGENITAL INFECTION- CMV, rubella, toxoplasmosis
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114
Q

What is symmetric growth restriction?

A

Where the entire body is proportionally small. It is early onset IUGR and is usually associated with chromosomal abnormalities.

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115
Q

What is asymmetric growth restriction?

A

An undernourished fetus who is compensating by directing most of its energy to maintaining the growth of the vital organs (e.g. brain and heart) at the expense of liver, fat and muscle.

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116
Q

What is the head-sparing effect?

A

Sign of asymmetric growth restriction wherein the baby has a normal head size with small abdominal circumference and thin limbs.
This is usually secondary to placental insufficiency

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117
Q

Management for IUGR (FGR)

A
  • Early identification
  • Intensive foetal monitoring
  • Continue the pregnancy safely for as long as possible- this will decrease prematurity complications but deliver before the fetus is compromised.
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118
Q

What is the prognosis for IUGR (FGR)?

A
  • Most go on to grow normally in infancy and childhood
  • 1/3 of IUGR children will not reach their predicted adult height
  • There may be experienced childhood attention and performance deficits.
  • There may be higher rate of coronary heart disease, high blood pressure, high cholesterol concentrations and abnormal glucose-insulin metabolism.
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119
Q

What is the incidence for multiple pregnancies?

A

TWINS- 15:1000
TRIPLETS- 1:5000
QUADRUPLETS: 1: 360,000

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120
Q

What are some risk factors for multiple pregnancies?

A
  • Previous multiple pregnancy
  • Family history
  • Increasing parity
  • Increasing maternal age
  • Ethnicity
  • Assisted reproduction
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121
Q

What are the signs and symptoms of a multiple pregnancy?

A
  • Hyperemsis gravidarum
  • Uterus is larger than expected for dates
  • Three or more fetal poles may be palpable
  • Two fetal hearts may be heard on auscultation
  • Majority are diagnosed on USS at the dating/ nuchal translucency scan
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122
Q

Considerations for antenatal care for multiple pregnancies…

A
  • Consultant- led care
  • Establish chorionicity (whether or not the babies share a placenta)
  • Routine use of iron and folate supplements
  • A detailed anomaly scan
  • More frequent antenatal checks because of increased risk of pre-eclampsia
  • Discuss mode of delivery
  • Establish presentation of leading twin
  • Consider delivery (induction) at 38 weeks
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123
Q

What are the maternal risks/complications of multiple pregnancy?

A
  1. Hyperemesis gravidarum
  2. Anaemia
  3. Pre-eclampsia (5x greater risk)
  4. Gestational diabetes
  5. Polyhydramnios
  6. Placenta praaevia
  7. Antepartum and postpartum haemorrhage
  8. Operative delivery
  9. Psychosocial- financially, breastfeeding, postnatal depression incidence increases
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124
Q

What are the foetal risks/complications of multiple pregnancy?

A
  • Increased risk of miscarriage (especially with monochromatic twins)
  • More common congenital abnormalities (neural tube defects, cardiac abnormalities, gastrointestinal atresia)
  • IUGR
  • Preterm labour (main cause of perinatal morbidity and mortality- 40% twins deliver before 37 wks, 10% deliver before 32)
  • Increased risk of intrauterine death- (8:1000 singles, 31:1000 twins, 84:1000 triplets)
  • Increased perinatal mortality
  • Increased risk of disability (due to preterm and low birth weight)
  • increased incidence of cerebral palsy
  • Vanishing twin syndrome (one twin reabsorbed at early gestation)
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125
Q

What is twin to twin transfusion syndrome?

A

There is a vascular anastomoses within the placenta which redistributes the foetal blood- i.e. blood from the ‘donor’ twin is transfused to the ‘recipient’ twin.

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126
Q

What are the clinical features of the ‘donor’ twin in twin-twin transfusion syndrome?

A
  • Hypovolaemic and anaemia
  • Oligohydramnios (appears ‘stuck’ to the placenta or uterine wall)
  • Growth restriction
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127
Q

What are the clinical features of the ‘recipient’ twin in twin-twin transfusion syndrome?

A
  • Hypervolaemic and polycythaemic
  • Large bladder and polyhydramnios
  • Evidence of foetal hydrops (ascites, pleural and pericardial effusions)

this twin is more at risk than the donor twin!

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128
Q

What are the four main types of hypertensive disease in pregnancy?

A
  1. PREGNANCY INDUCED HYPERTENSION
  2. CHRONIC HYPERTENSION
  3. POSTPARTUM HYPERTENSION
  4. PRE-ECLAMPSIA
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129
Q

Features of pregnancy induced hypertension.

A
  • It is characterized as HTN in the second half of pregnancy in the absence of proteinuria
  • It affects 6-7% of pregnancies with an increased risk of going on to develop pre-eclampsia
  • The risk increases with earlier onset of hypertension
  • Delivery should be aimed at EDD
  • BP usually returns to pre-pregnancy limits within 6 weeks of delivery.
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130
Q

Features of chronic hypertension in pregnancy.

A
  • Complicates 3-5% of pregnancies
  • Pregnant women with high ‘booking’ BP (130-140/80-90) are likely to have chronic hypertension
  • Carries an increased risk of pre-eclampsia
  • Deliver should be aimed at EDD

Now more common due to older pregnant population

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131
Q

Features of postpartum hypertension

A
  • New HTN can arise in the postpartum period.

- It is important to determine whether it is physiological, pre-existing chronic HTN or new onset pre-eclampsia.

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132
Q

What is pre-eclampsia?

A
  • BP >140/90 and >300mg proteinuria in a 24 hour collection.
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133
Q

What is the classification for mild pre-eclampsia?

A

Proteinuria and mild/moderate hypertension

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134
Q

What is the classification for moderate pre-eclampsia?

A

Proteinuria and severe hypertension with no maternal complications.

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135
Q

What is the classification for severe pre-eclampsia?

A

Proteinuria and any hypertension <34 weeks or with maternal complications

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136
Q

What are some of the risk factors for pre-eclampsia?

A
  • Previous severe/ early onset pre-eclampsia
  • Age: >40 or teenager
  • Family History (mother/sister)
  • Obesity (BMI >30)
  • Primiparity
  • Multiple pregnancy
  • Long birth interval (>10 years)
  • Foetal hydrops
  • Hydatidiform mole (uterine growth that forms at the start of pregnancy)
  • Pre-existing medical conditions: HTN, renal disease, diabetes, thrombophilias, connective tissue disease, APA.
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137
Q

What are the symptoms of pre-eclampsia?

A
  1. Headache (esp. frontal)
  2. Visual disturbance (esp. flashing lights)
  3. Epigastric or RUQ pain
  4. Nausea and vomiting
  5. Rapid oedema (especially in the face)

symptoms usually manifest in severe disease

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138
Q

What are the signs of pre-eclampsia?

A
  • HTN
  • Proteinuria
  • Facial oedema
  • Epigastric RUQ tenderness
  • Confusion
  • Hyperreflexia and/or clonus (sign of cerebral irritability)
  • Uterine tenderness or vaginal bleeding from placental abruption
  • Foetal growth restriction on USS esp. if <36 wks
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139
Q

What lab investigations are performed in pre-eclampsia?

A
  1. FBC - will show high Hb due to haemoconcentration, thrombocytopaenia, anaemia
  2. COAGULATION PROFILE- will show prolonged PT and APTT
  3. BIOCHEMISTRY- will show high urate, high urea and creatinine, abnormal LFTS (raises transaminases), high LDH )marker of haemolysis), high proteinuria (>300mg in 24 hours)
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140
Q

What are the complications associated with pre-eclampsia?

A
  • Eclampsia- which is tonic/clonic seizure in association with pre-eclampsia
  • HELLP- haemolysis, elevated liver enzymes and low platelets.
  • Cerebral haemorrhage
  • Disseminated intravascular coagulation (DIC)
  • Renal failure
  • Placental abruption
  • Pulmonary oedema
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141
Q

What is the outpatient management plan for pre-eclampsia?

A

IF the BP is <160/<110 and can be controlled, there is no/low proteinuria (<300mg in 24 hrs) and the patient is asymptomatic…

  • warn about development of symptoms
  • 1-2 per week review of BP and urine
  • Weekly review of biochemistry
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142
Q

What is the management plan for mild-moderate pre-eclampsia?

A

IF BP is <160/<110 with proteinuria but there are no maternal complications

  • ADMISSION IS ADVISED
  • 4 hourly BP
  • 24 hour urine collection for protein
  • daily urinalysis
  • daily foetal assessment with CTG
  • regular blood tests (every 2-3 days)
  • regular ultrasound assessment (2/52 growth, 2/7 doppler/liquor volume depending on severity)
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143
Q

What is the management plan for severe pre-eclampsia?

A

IF BP >160/>110, with significant proteinuria (>1g/24h) and there are maternal complications

  • Commence BP control. Aim for <160/<110
  • Use NIFEDIPINE 10mg PO

If remains high after nifedipine

  • Start IV labetalol
  • Increase the infusion rate until the BP is adequately controlled
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144
Q

Which antihypertensives can be used in the management of pre-eclampsia?

A
  • Labetalol (po and IV)
  • Nifedipine
  • Methyldopa
  • Hydralazine (IV)
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145
Q

What is the cure for pre-eclampsia?

A

DELIVERY OF PLACENTA AND BABY

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146
Q

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

A
  • Worsening thrombocytopenia or coagulopathy
  • Worsening liver or renal function
  • Severe maternal symptoms
  • HELLP syndrome or eclampsia
  • Fetal distress
  • Reversed umbilical artery flow
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147
Q

How to manage pre-eclampsia in <34 weeks?

A
  • Follow management plan according to severity
  • pre-emptive steroids
  • although immediate delivery is the only cure, this can be delayed with intensive monitoring
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148
Q

What is pre-gestational diabetes?

A

Poor glycemic control.

It increases foetal and neonatal morbidity and mortality

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149
Q

What are the maternal complications of diabetes in pregnancy?

A
  • UTI
  • Pregnancy-induced HTN or pre-eclampsia
  • Obstructed labour
  • Operative deliveries (CS and assisted vaginal deliveries)
  • Increased retinopathy
  • Increased nephropathy
  • Cardiac disease
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150
Q

What are the foetal complications of diabetes in pregnancy?

A
  • Miscarriage
  • Congenital abnormalities (neural tube defects, microcephaly, cardiac abnormalities, sacral genesis, renal abnormalities)
  • Preterm labour
  • IUGR
  • Unexplained IUD
  • Macrosomia
  • Polyhydramnios
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151
Q

What are the neonatal complications of diabetes in pregnancy?

A
  • Polycythaemia
  • Birth trauma (shoulder dystocia, fractures, Erb’s palsy, asphyxia)
  • Hypocalcemia
  • Hypoglycaemia
  • Hypomagnesaemia
  • Hypothermia
  • Jaundice
  • Cardiomegaly
  • Respiratory distress syndrome
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152
Q

What is the postpartum care for those with pre-existing diabetes?

A

Remember that insulin requirements fall dramatically after delivery of the placenta.

  • Change back to SC insulin when eating and drinking
  • roughly half the prepregnancy dose of SC insulin
  • Aim for BM 4-9mmol/L in the postpartum period
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153
Q

What are the risk factors for gestational diabetes (GDM)?

A
  • Previous GDM
  • Family history of diabetes
  • Previous macrocosmic baby
  • Previous unexplained stillbirth
  • Obesity (BMI >30)
  • Glycosuria on more than one occasion
  • Polyhydramnios
  • Large for gestational age fetus in current pregnancy
  • Ethnicity
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154
Q

What is involved in the oral glucose tolerance test (OGTT)?

A

There has to be an overnight fasting period (8 hours minimum)

  • only water may be consumed
  • no smoking

Patient has a 75g glucose load in 250-300ml of water.
Plasma glucose is measured at fasting and at 2 hours

In diabetes:
fasting glucose >7.0mmol/L
2hr glucose >11.1 mol/L

In impaired glucose tolerance:
fasting glucose <7.0mmol/L
2hr glucose >7.8 but <11.1mmol/L

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155
Q

What is the management for gestational diabetes?

A
  • Involvement of the multidisciplinary team
  • Measure glucose QDS

First line treatment should be diet

  • aim for normoglycemia and avoid ketosis
  • weight should remain steady if diet followed
  • compliance is often poor- dietician may help
  • serial USS scanning
  • Start insulin if:
    pre-meal glucose is >6mmol/l
    1hr postprandial glucose >7.5mmol/L
    AC > 95th percentile despite apparent good control
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156
Q

What is the management for postpartum gestational diabetes?

A
  • Stop insulin and glucose infusions
  • Check glucose prior to discharge to ensure normal
  • Arrange OGTT at 6 wks post partum
  • Education
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157
Q

Management/care in pre-gestational diabetes

A
  • Check folic acid, as it can increase risk of neural tube defects (therefore start on 5mg)
  • consider nuchal translucency testing rather than serum screening as this is affected by diabetes
  • thorough anomaly scan
  • fetal echocardiography at 20-24 weeks
  • serial USS every 2-4 weeks to detect polyhydramnios, macrosomia or IUGR
  • be aware of hypoglycemia and educate mother and family
  • Vaginal delivery preferred
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158
Q

How is glucose controlled during labour?

A

If patient is diet controlled: check glucose hourly- if >6mmol/l start sliding scale

if patient is insulin dependent: continue SC insulin until in established labour, then convert to insulin sliding scale.

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159
Q

What is the leading cause of maternal morbidity and mortality?

A

VTE- in the form of DVT and PE

antenatal DVT is more common than postpartum DVT

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160
Q

Inherent pregnancy associated risk factors for VTE

A
  • Venous stasis in the lower limbs
  • Possible trauma to the pelvic veins at time of delivery
  • Changes in the coagulation system including : increase in procoagulant factors (factors X,VIII and fibrinogen), decrease in endogenous anticoagulant activity, suppression of fibrinolysis, significant decrease in protein S activity.
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161
Q

Pre-existing risk factors for VTE

A
  • Previous VTE
  • Congenital thrombophilia (deficiency of antithrombin, protein C, protein S), factor V Leiden, prothrombin gene variant
  • Acquired thrombophilia (lupus anticoagulant, anticardiolipin antibodies)
  • Age >35
  • Obesity (BMI >30)
  • Parity >4
  • Gross varicose veins
  • Paraplegia
  • Sickle cell disease
  • Inflammatory disorders e.g. IBD
  • Medical disorders e.g. nephrotic syndrome, cardiac diseases
  • Myeloproliferative disorders- essential thrombocythaemia, polycythemia vera
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162
Q

What are the new onset/ transient risk factors for VTE in pregnancy?

A
  • Ovarian hyperstimulation syndrome
  • Hyperemesis
  • Dehydration
  • Long-haul travel
  • Severe infection e.g. pyelonephritis
  • Immobility
  • Pre-eclampsia
  • Prolonged labour
  • Midcavity instrumental delivery
  • Excessive blood loss
  • Surgical procedure in pregnancy or puerperium, e.g. evacuation of retained products of conception, postpartum sterilization
  • Immobility after delivery
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163
Q

What are the preventative measures for VTE in pregnancy?

A

LMWH

In previous VTE: LMWH for 6 wks postpartum only

In previous recurrent VTE/previous VTE and family history: LMWH antenatally, and for 6 wks postpartum

In previous VTE and thrombophilia: LMWH antenatally and for 6 wks postpartum

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164
Q

Factors for giving LMWH postpartum

A
  • Age > 35 years

- BMI >30 or body weight >90kg

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165
Q

What investigations are used in diagnosing VTE in pregnancy?

A
  • Lower limb dopplers in suspected DVT

- CXR, CTPA and VQ scan in suspected PE

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166
Q

D-dimers and pregnancy?

A

D-dimer can be elevated due to physiological changes , therefore a positive d-dimer may not be consistent with VTE

BUT

Low D-dimer level is likely to suggest that there is no VTE

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167
Q

Management for VTE in pregnancy

A

LMWH
Twice daily dosage regimen for LMWH:
- tinzaparin, enoxaparin 1mg/kg twice daily
- dalteparin 100units/kg twice daily (max of 18000U/24h)

STOP THE NIGHT BEFORE DELIVERY

OR

UFH (unfractionated heparin)

  • Loading dose of 5000IU, followed by continuous IV infusion of 1000/2000 IU/h with an initial infusion concentration of 1000IU/ml
  • Measure APTT level 6 hours after the loading dose, then at least daily.

Warfarin can be used postnatally and is safe for breast-feeding.

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168
Q

What are the reasons for VBAC (vaginal birth after caesarean section)?

A
  1. Vaginal birth has physical and psychological benefits for both mum and baby
  2. SAFETY- VBAC can be safer for the woman the repeat caesarean.
  3. Previous vaginal delivery is associated with planned VBAC success and reduced risk of rupture.
  4. Intrapartum infant death is rare
  5. Success rates are seemingly not affected compared to other births
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169
Q

What are the reasons against VBAC (vaginal birth after caesarean section)?

A
  1. Must be on labour ward (must deliver where there is immediate access to CS and on site blood transfusion)
  2. Uterine rupture
  3. Must be hooked up to a CTG the whole time
  4. Contraindicated if you have had a ‘classic cut’ (rare type of CS)
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170
Q

What are the seven main stages in the mechanism of labour?

A
  1. ENGAGEMENT AND DESCENT
  2. FLEXION
  3. INTERNAL ROTATION OF THE HEAD
  4. EXTENSION OF THE HEAD
  5. RESTITUTION
  6. INTERNAL ROTATION OF THE SHOULDERS
  7. LATERAL FLEXION
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171
Q

What occurs during ENGAGEMENT AND DESCENT?

A
  • Contraction and retraction of the uterine muscles allows less room in the uterus
  • Exerting pressure on the fetus to descend
  • Head enters the pelvis in the OCIPITOTRANSVERSE position
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172
Q

What occurs during FLEXION?

A
  • Pressure exerted down the foetal axis will increase flexion
  • Resulting in smaller presenting diameters that will negotiate the pelvis more easily
  • At onset of labour the SUBOCIPITOFRONTAL DIAMETER is presenting (10cm)
  • With greater flexion the SUBOCIPITOBEGMATIC (9.5cm) presents.
  • The occiput becomes the leading part
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173
Q

What occurs during INTERNAL ROTATION OF THE HEAD?

A
  • Leading part is pushed downwards onto the pelvic floor
  • This muscular resistance from the pelvic floor brings about rotation
  • Causes slight twist in neck, as it is no longer in alignment with the shoulders
  • The anterior-posterior diameter of the head now lies in the widest diameter of the pelvic outlet
  • The occiput slips beneath the sub-pubic arch and crowning takes place when the widest transverse diameter is born.
  • Whilst flexion is maintained the suboccipitobregmatic diameter distends the vaginal orifice.
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174
Q

What occurs during EXTENSION OF THE HEAD?

A
  • Once crowning has occurred the foetal head can extend
  • Pivoting on the sub-occipital region around the pubic bone
  • The sinciput, face and chin sweep the perineum and are born
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175
Q

What occurs during RESTITUTION?

A
  • The twist in the neck of the fetus which results from the internal rotation is corrected by an untwisting movement.
  • Bringing the head and neck back into alignment
  • The occiput moves 1/8th (45 degrees) of a circle towards the side which it started
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176
Q

What occurs during the INTERNAL ROTATION OF THE SHOULDERS?

A
  • The anterior shoulder is the first to meet the pelvic floor- rotates anteriorly to lie under the symphysis pubis
  • This can clearly be seen as the head turns at the same time- external rotation of the head
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177
Q

What occurs during LATERAL FLEXION?

A
  • The anterior shoulder is born first
  • The anterior should slips beneath the sub-pubic arch and the posterior shoulder passes over the perineum.
  • The remainder of the body is born by lateral flexion as the spine bends sideways through the birth canal- following the curve of carus.
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178
Q

What are Braxton-Hicks?

A

Mild, irregular, non-progressive contractions that may occur from 30 wks (more common after 36) and are often confused with labour.

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179
Q

What characterizes contractions in labour?

A
- PAIN
The tend to have a gradual increase in:
- frequency
- amplitude
- duration
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180
Q

What denotes the first stage of labour?

A

Onset of labour to full dilatation of the cervix, divided into two phases:

  • LATENT PHASE
  • ACTIVE/ ESTABLISHED PHASE
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181
Q

What occurs during the LATENT phase of 1st stage of labour?

A

It is the period of time (not necessarily continuous) where there are painful contractions and some cervical change including effacement and dilatation up to 4cm.

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182
Q

What occurs during the ACTIVE/ ESTABLISHED phase of 1st stage of labour?

A

Regular contractions (5mins apart and getting closer) and progressive dilatation from 4cm to full dilatation (10cm)

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183
Q

Expected progression of dilatation in labour?

A

For primigravida- 0.5cm/h once in established labour

For multiparous- 0.5cm/h

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184
Q

What are the three P’s?

A
  • POWER
  • PASSENGER
  • PASSAGE
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185
Q

What denotes slow progress in the active phase of labour?

A

<2cm dilatation in 4 hours or a slowing in progress in parous women

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186
Q

What are the common causes of failure to progress in labour?

A

POWER- insufficient uterine action
PASSAGE- cephalo-pelvic disproportion, possible role of cervix
PASSENGER- fetal size, disorder of rotation, disorder of flexion

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187
Q

What is the management for failure to progress in labour?

A
  • Amniotomy (artificial rupturing of the membrane) and reassess in 2 hours
  • Amniotomy and oxytocin infusion and reassess in 2 hours
  • Lower segment CS (if there is fetal distress)
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188
Q

What denotes the second stage of labour?

A

From full cervix dilatation until the baby is born

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189
Q

What is PASSIVE second stage?

A

When there is full dilatation of the cervix before/without involuntary expulsive contractions

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190
Q

What is ACTIVE second stage?

A

When the mother starts expulsive efforts using her abdominal muscles with the Valsalva manoeuvre to ‘bear down’.

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191
Q

How is perineal distention slowed?

A

A pad may be used to support the perineum and cover the anus, while another hand maintains flexion and controls the rate of delivery of the head.

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192
Q

Indication for episiotomy?

A

If there is concern that the perineum is tearing towards the anal sphincter

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193
Q

Mechanisms of the second stage of labour

A
  • as the head comes down it distends the perineum and anus
  • with next contraction gentle traction guides the head towards the perineum until the anterior shoulder is delivered under the subpubic arch
  • gentle traction upwards and anteriorly helps to deliver the posterior shoulder and the remainder of the trunk
  • the cord is double-clamped and cut
  • condition of the baby is assessed using the APGAR scoring system and if all is well, baby is handed to mother as soon as possible
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194
Q

What denotes delay in 2nd stage?

A

Primaparous- Birth should take place within 3 hours of the start of 2nd stage (and within 2 hours of actively pushing)

Multiparous- Birth should take place within 2 hours of start of 2nd stage (and within 1 hour of actively pushing)

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195
Q

Management for delay in 2nd stage for primiparous women?

A
  • VE should be offered
  • amniotomy recommended
    if not delivered in 2 hours, obstetrician review to consider instrumental delivery or CS
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196
Q

Management for delay in 2nd stage for multiparous women?

A
  • if not delivered in 1 hour, obstetrician review to consider instrumental delivery or CS
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197
Q

What denotes the third stage of labour?

A

Duration from delivery of the baby to delivery of the placenta and membranes.
Can be divided into ACTIVE MANAGEMENT and PHYSIOLOGICAL MANAGEMENT

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198
Q

Active management of stage 3 labour:

A
  • This is prolonged if not completed within 30 mins
  • Involves the routine use of uterotonic drugs
  • Early clamping and cutting of the cord
  • Controlled cord traction
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199
Q

Physiological management of stage 3 labour:

A
  • Prolonged if not completed within 60 mins
  • No routine use of uterotonic drugs
  • No clamping of the cord unless pulsation has ceased
  • Delivery of the placenta by maternal effort
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200
Q

When would you change from physiological -> active management during stage 3 labour?

A
  1. Haemorrhage
  2. Failure to deliver the placenta within 1 hour
  3. Maternal desire to shorten stage 3
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201
Q

Which key components are assessed during vaginal examination to assess progress?

A

CERVIX

  • position
  • consistency
  • effacement
  • dilatation
  • Application of cervix to presenting part
  • Membranes
  • Presenting part
  • Descent of presenting part
  • Position and attitude flexion
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202
Q

What is assessed during routine monitoring of labour?

A
  • OBS- pulse, BP, temp, urinalysis
  • VAGINAL LOSS- liquor (clear, meconium/blood stained), fresh blood
  • CONTRACTION FREQUENCY, STRENGTH AND LENGTH
  • ABDOMINAL PALPATIONS AND VE to determine progress
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203
Q

What is a partogram and what is charted on one?

A

A pectoral record of labour

  1. Cervical dilatation and descent of the head
  2. Frequency of contractions
  3. Fetal heart rate
  4. Liquor color
  5. Maternal observation
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204
Q

What are the primary modes of foetal injury during labour?

A
  • Hypoxia
  • Meconium aspiration
  • Trauma
  • Infection/ inflammation
  • Blood loss
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205
Q

What is foetal distress?

A

Hypoxia that may result in foetal damage or death if not reversed or the fetus is delivered urgently.

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206
Q

What can be seen as high risk situations in labour?

A
  1. FOETAL CONDITIONS- e.g. IUGR, prolonged pregnancy
  2. MEDICAL COMPLICATIONS- e.g. diabetes, preeclampsia
  3. INTRAPARTUM FACTORS- long labour, meconium, maternal fever
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207
Q

What are two main foetal monitoring methods?

A
  1. INTERMITTENT AUSCULTATION

2. INSPECTION FOR MECONIUM

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208
Q

What is the normal foetal heart rate?

A

100-160 bpm

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209
Q

How to manage if foetal blood sample is abnormal?

A

Deliver by the quickest route:

  • Caesarean section if first stage
  • Instrumental vaginal delivery if second stage and criteria met
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210
Q

In low risk women, what does foetal monitoring entail?

A

Intermittent auscultation of the foetal heart using a Sonicaid/Doppler or Pinard

  • at least every 15min in the first stage
  • every 5 minutes or after every other contraction in the 2nd stage
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211
Q

In high risk women, what does foetal monitoring entail?

A

Continuous monitoring using a CTG

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212
Q

What are the main components of a cardiotocograph?

A

DR C BRAVADO

DR- Determine Risk
C- Contractions
BR- Baseline Rate
A- Accelerations
V- Variability
D- Deceleration
O- Overall impression: normal/ reassuring
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213
Q

What does variability in FHR indicate?

A

VEAL - CHOP

Variable- Cord compression
Early Deceleration- Head compression
Accelerations- OK (this is good and reassuring)
Late Deceleration- Placenta (indicates placental insufficiency and poor perfusion).

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214
Q

What should contractions look like on the CTG?

A

Should measure at 4-5/10mins in labour

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215
Q

What is the baseline rate on CTG?

A

This is the mean level of the FHR when it is stable, after exclusions of accelerations and decelerations. (should be between 100-160)

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216
Q

What is baseline variability on CTG?

A

The degree to which the baseline varies, i.e. the bandwidth excluding accelerations and decelerations.

A variability of +5 bpm is normal.
<5 bpm is reduced
5-25 is very sensitive to hypoxia

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217
Q

What is acceleration on CTG?

A

A transient rise in FHR by at least 15 beats over the baseline lasting for 15 seconds or more. It is ALWATS GOOD.

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218
Q

What is deceleration on CTG?

A

A reduction in the baseline FHR by 15 beats or more for more than 15 seconds.

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219
Q

Management of a worrying CTG?

A
  • Change maternal position- left lateral (reduces aortocaval compression)
  • Give fluids- to avoid dehydration
  • Foetal scalp stimulation
  • Foetal blood sample
  • Delivery?
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220
Q

What are some indications for fetal blood sampling?

A
  • Diagnosing fetal hypoxia

- If worried about CTG and delivery is not imminent

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221
Q

How does fetal blood sampling occur?

A

It is an INVASIVE procedure

The woman should be in LEFT LATERAL position and at least 3CM DILATED.

  • Insert amnioscope
  • Remove probe
  • Clean scalp
  • Stab with blade and collect with capillary tube
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222
Q

What do the measurements of fetal pH indicate?

A

> 7.25 Normal
7.20-7.25 Borderline- repeat in 30 mins if CTG not ok
<7.20 DELIVER!

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223
Q

What is a fetal scalp electrode?

A

It is used for monitoring the fetal surveillance when the FHR is non-reassuring, or external FHR monitoring is difficult due to maternal body habitus or excessive foetal movement

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224
Q

What are problems/obstacles associated with the use of the fetal scalp electrode?

A
  • Poor contact with abdominal transducer
  • High BMI
  • Twins
  • Abdominal scarring
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225
Q

What are the main points of maternal monitoring?

A
  1. PULSE
  2. BP
  3. TEMPERATURE
  4. RESPIRATORY RATE
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226
Q

What is included in care in labour for the mother?

A

EATING AND DRINKING

  • encourage women to drink throughout
  • light meals when desired

BLADDER CARE

  • encourage women to pass urine regularly
  • may need a catheter if unable

PAIN RELIEF
- discuss options including any risks/ benefits and provide when requested

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227
Q

What are the factors that affect pain in labour?

A
  1. Position of the baby
  2. Size of baby
  3. Pelvic anatomy
  4. Strength of contraction
  5. Complications- APH, uterine rupture, trauma
  6. Previous experience and expectations
  7. Other factors- anxiety, fear of pain, social factors, educational background etc.
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228
Q

What are the pain pathways in labour?

A
  1. NOCICEPTORS
  2. A FIBRES
  3. C FIBRES
  4. DORSAL HORN
  5. LATERAL SPINOTHALAMIC TRACT
  6. THALAMUS
  7. SENSORY CORTEX
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229
Q

What are the causes of pain during the 1st stage of labour?

A
  • Uterine contractions
  • Tightenings
  • Dilatation of the lower segment of the uterus and cervix
  • Visceral pain- colicky, poorly localised
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230
Q

How is pain during the 1st stage of labour carried?

A

Via T10-L1 ROOTS

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231
Q

What are the causes of pain during the 2nd stage of labour?

A
  • Pain of the first stage continues
  • Dilation and pressure on pelvic organs and pelvic floor structures
  • Pudendal nerves
  • Somatic pain, sharp- well localized
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232
Q

How is pain during the 2nd stage of labour carried?

A

Via S2- S4 ROOTS

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233
Q

What are the physiological responses to pain during labour?

A
  • Release of stress hormones (cortisol)
  • Increased oxygen consumption
  • Hyperventilation
  • Increased blood pressure
  • Increased cardiac output
  • Increased vascular resistance
  • Delayed gastric emptying
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234
Q

What are the non-pharmacological methods for pain management in labour?

A
  • Education regarding what to expect- reduce fear and the sense of loss of control
  • Good birth partner
  • Warm bath, acupuncture, hypnosis aromatherapy and homeopathy
  • Transcutaneous Electrical Nerve Stimulation (TENS)
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235
Q

What are the pharmacological methods for pain management in labour?

A
  1. INHALATIONAL (Entonox- nitrous oxide)
  2. PARACETAMOL
  3. OPIOID
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236
Q

What is Entonox?

A
  • Pharmacological analgesia for labour
  • premixed nitrous oxide and oxygen as a 50:50 mixture.
  • Works on NMDA receptors

Side effects

  • feeling faint
  • nausea
  • vomiting
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237
Q

Which opioids are contraindicated during labour?

A
  • MORPHINE
  • CODEINE
  • FENTANYL
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238
Q

Which opioids are used for analgesia in labour?

A

DIAMORPHINE

  • 1st line
  • 2.5-5mg IM

PETHIDINE

  • 50-150mg
  • the onset of action is 15-20min
  • lasts 3-4h and can be repeated
  • Usually given with an antiemetic
  • CAN CAUSE NEONATAL RESPIRATORY DEPRESSION

MEPTAZINOL
- Onset of action starts in 15 mins and lasts for 2-7 hours

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239
Q

What regional anesthesia is used during labour?

A

PUDENDAL NERVE BLOCK

  • used for operative vagina delivery
  • Lidocaine (lignocaine) is injected 1-2cm medially below the right and left ischial spines
  • administered transvaginally with a specially designed pudendal needle.
LOCAL ANAESTHETIC (LIDOCAINE)
- Infiltrated in the perineum before performing an episiotomy at the time of delivery, or before suturing tears and episiotomies.
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240
Q

Where is the epidural space?

A

Lies between spinal dura and the vertebral canal

Contains spinal nerve roots as well as spinal arteries and extradural veins.

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241
Q

What is the distance between the skin and the epidural space in the lumbar region in adults?

A

4-5 cm

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242
Q

What is a combined spinal epidural (CSE)?

A

Intrathecal injection and epidural catheter placement
Preferred in advanced labour

  • Complications of this:
  • infection
  • intrathecal migration of catheter
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243
Q

Why would the use of an epidural in labour be contraindicated?

A
  • Bleeding disorders
  • Local/systemic infection
  • Spinal surgery
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244
Q

What are the advantages of an epidural?

A
  1. Provides effective analgesia in labour
  2. Reduced maternal secretion of catecholamines, which benefits the fetus
  3. Can be used when topped up for an operative delivery and for any complication of the 3rd stage of labour, e.g. retained placenta/ repair of perineal tears
  4. Can provide effective postoperative analgesia
  5. Can be used as a additional method of controlling blood pressure in pre-eclampsia.
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245
Q

What are the disadvantages of an epidural?

A
  1. Failure to site, or a patchy incomplete block
  2. Hypotension from sympathetic blockade
  3. Tenderness over insertion site
  4. Decreased mobility
  5. Inadvertent dural puncture (may develop a postural puncture headache characterized by increased pain on sitting up or standing and may need treatment with an epidural blood patch.
  6. Respiratory depression (from catheter migrating into subarachnoid space followed by bolus of local anaesthetic OR from accumulation of epidural administered opiates)
  7. Increased risk of operative delivery
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246
Q

What are some of the controversies/ myths associated with epidural?

A
  • Epidural prolongs labour
  • Increases incidence of Caesarean section
  • Causes chronic backache
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247
Q

What are the most common indications for the induction of labour?

A
  • Healthier outcome for mother or fetus than if birth is delayed
  • Prolonged pregnancy
  • Suspected IUGR
  • Hypertension and pre-eclampsia
  • Planned time of delivery- baby’s best interests
  • Only if vaginal delivery is deemed appropriate
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248
Q

What are the obstetric indications for the induction of labour?

A
  • Uteroplacental insufficiency
  • Prolonged pregnancy
  • IUGR
  • Oligo or anhydramnios
  • Abnormal uterine or umbilical artery doppler
  • Non-reassuring CTG
  • Prelabour rupture of membranes (give steroids until delivery)
  • Severe pre-eclampsia or eclampsia after maternal stabilization
  • Diabetes (5x risk of still birth- induce at 38 weeks)
  • Intrauterine death of the fetus
  • Unexplained antepartum hemorrhage at birth
  • Chorioamnionitis
  • Obvious fetal abnormality
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249
Q

What are the maternal indications for the induction of labour?

A
  • Severe hypertension
  • Uncontrolled diabetes mellitus
  • Renal disease with deteriorating renal function
  • Malignancies (to facilitate definitive therapy)
  • Cardiac abnormalities
  • Aged >40, induce at term
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250
Q

What are the absolute contraindications for inducing labour?

A

ACUTE FETAL COMPROMISE
UNSTABLE LIE
PLACENTA PRAEVIA
PELVIC OBSTRUCTION

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251
Q

What are the relative contraindications for inducing labour?

A

PREVIOUS C SECTION
BREECH
PREMATURITY
HIGH PARITY

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252
Q

What is the Bishop’s score?

A

A pre-labour scoring system to assess whether or not induction of labour is necessary.

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253
Q

What should be checked before induction?

A
  • Lie and position of the fetus
  • Volume of amniotic fluid
  • Tone of the uterus
  • Ripeness of the cervix- this is the best indicator for readiness for induction. If the Bishop’s score is >8, the probability of successful delivery with induction is the same as spontaneous onset of labour.
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254
Q

What is the mechanical way to induce cervical ripening?

A

by performing the STRETCH AND SWEEP

all women should be offered this before formal induction

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255
Q

What is the pharmacological way to induce cervical ripening?

A

By using PROSTAGLANDIN E2 in the form of Propess

  • This is the preferred agent for cervical ripening
  • Its is given TRANSVAGINALLY into the POSTERIOR FORNIX.
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256
Q

What is an amniotomy?

A
  • It is the artificial rupture of membranes (ARM) using an amnihook.
  • It releases prostaglandins which leads to cervical ripening and myometrial contractions.
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257
Q

When would you use oxytocin infusion following ARM?

A

If there are no changes after 2 hours following ARM

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258
Q

Does ARM increase the rate of going into established labour?

A

Yes, 88% of patients will go into established labour within 24 hours of ARM alone.

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259
Q

What precautions should be taken when using prostaglandins for labour?

A
  1. CTG should be performed 30mins before and after prostaglandin insertion.
  2. VE should be performed 6 hours after prostaglandin insertion, and if the cervix is still not favorable, another dose may be administered.
  3. Oxytocin should not be started for 6 hours after prostaglandin insertion to avoid the risk of uterine hyperstimulation.
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260
Q

How should Syntocinon be used?

A
  • Started on low dose (1-4mU/min)
  • Increase every 30mins (usually doubled) to achieve optimal contractions (3-4 every 10mins lasting 40-60sec each)
  • Infusion pumps should be used to carefully control the amount given to avoid uterine hyperstimulation.
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261
Q

What should be considered when Syntocinon is used?

A

The sensitivity of the myometrium to oxytocin increases during labour and it may be necessary to decrease the rate of infusion of syntocinon as labour advances!

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262
Q

What are the complications associated with inducing labour?

A
  • It precipitates delivery
  • Increases risk of operative delivery
  • Can cause uterine hypertonia with possible rupture
  • Amniotic fluid embolus
  • Prematurity (which may be iatrogenic or unintentional)
  • Cord prolapse with rupture of membrane, if presenting part (baby head) is not engaged
  • Caesarean section due to failed induction
  • Atonic postpartum hemorrhage
  • Intrauterine infection with prolonged induction
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263
Q

What are the side effects of the pharmacological agents used in the induction of labour?

A
  • pain or discomfort
  • uterine hyperstimulation
  • fetal distress
  • uterine rupture
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264
Q

What is a rare side effect of prostaglandin use in the induction of labour?

A

NON-SELECTIVE STIMULATION OF OTHER SMOOTH MUSCLE leading to:

  • nausea and vomiting
  • diarrhoea
  • bronchoconstriction
  • maternal pyrexia due to the effect of thermoregulation in the hypothalamus
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265
Q

What is a rare side effect of oxytocin use in the induction of labour?

A

DILUTIONAL HYPONATRAEMIA

  • oxytocin has the properties of antidiuretic hormone (ADH), therefore U+Es should be checked in oxytocin use for >12 hours
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266
Q

What occurs if a labour is not progressing in 2nd stage?

A

If after 2 HOURS of passive descent and PUSHING FOR 1 HOUR, check if the baby is above or below the ischial spines.

If ABOVE: Caesarean section
If BELOW: Instrumental delivery

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267
Q

What is malposition in abnormal labour?

A

Malpositions are abnormal positions of the vertex of the fetal head (using the occiput as reference point) relative to the maternal pelvis.

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268
Q

What is the normal position in labour?

A

The vertex is the presenting part
- fetal occiput transverse in the maternal pelvis
with descent the fetal head rotates so that:
- fetal occiput is anterior in the maternal pelvis

There should also be a WELL FLEXED VERTEX with the occiput lower in the vagina than the sinciput.

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269
Q

What is the most common malposition in labour?

A

OCCIPITO-POSTERIOR

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270
Q

What is the occipito-posterior position in labour?

A
  • Initially engages normally but then the occiput rotates posteriorly.
  • It results from a poorly flexed vertex. The anterior fontanelle is felt anteriorly.
  • This may occur because of a flat sacrum, poorly flexed head or weak uterine contractions.
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271
Q

What is the management for an occipito-posterior position in labour?

A
  • Close maternal and fetal monitoring required due to long labour
  • Epidural recommended
  • Adequate fluids for mother
  • Discourage mother from pushing until full dilatation
  • Forceps/ CS may be required
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272
Q

What is the occipto-tansverse position in labour?

A
  • The head initially engages correctly but fails to rotate and remains in a transverse position.
  • If the second stage is reached (i.e. dilation up to 10cm), had must be manually rotated with Kielland’s forceps or delivered using vacuum extraction.

HOWEVER
This is inappropriate if there is any fetal acidosis because of the risk of cerebral haemorrhage, therefore trial forceps delivery in theatre to accommodate for emergency CS

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273
Q

What are face presentations in labour?

A
  • Complete extension of the fetal head
    In the MENTO-ANTERIOR position, vaginal delivery should be achieved after a long labour
    In the MENTO-POSTERIOR position, CS is required
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274
Q

What is brown position in labour?

A
  • When the fetal head stays between full extension and full flexion- i.e. the largest diameter (MENTO-VERTEX) is presenting.
  • This is usually only diagnosed when labour is established
  • The anterior fontanelle and super orbital ridges are palpable on vaginal examination.
  • Until the head flexes, a vaginal delivery is not possible and CS is required.
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275
Q

What is a malpresentation in labour?

A

Presentations of the fetus other than vertex (other than the head), as the presenting part.

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276
Q

What are the two commonest types of malpresentation?

A

BREECH

TRANSVERSE LIE

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277
Q

What are the predisposing factors to malpresentation?

A
  1. PREMATURITY
  2. MULTIPLE PREGNANCY
  3. ABNORMALITIES OF THE UTERUS e.g. fibroids
  4. PARTIAL SEPTATE UTERUS
  5. ABNORMAL FETUS
  6. PLACENTA PRAEVIA
  7. PRIMIPARITY
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278
Q

What defines a BREECH presentation in labour?

A

This occurs when the baby’s buttocks lie over the maternal pelvis.

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279
Q

What can be found on examination of a breech presentation in labour?

A
  • lie is longitudinal
  • the head can be palpated at the fundus
  • the presenting part is not hard
  • the fetal heart is best heard high up on the uterus
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280
Q

What are the types of breech?

A
  • EXTENDED/ FRANK BREECH (70%)
    both legs extended with feet by head; presenting part is the buttocks
  • FLEXED/ COMPLETE BREECH (15%)
    legs flexed at the knees so that both buttocks and feet are presenting
  • FOOTLING/ INCOMPLETE BREECH (15%)
    one leg flexed and one extended
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281
Q

What are the risks associated with breech?

A
  • There is an increased risk of hypoxia and trauma in labour
  • There are neonatal and longer-term risks because:
    there is association with congenital abnormalities
    many preterm babies are breech at the time of delivery
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282
Q

What is the management for breech presentation in labour?

A

EXTERNAL CEPHALIC VERSION
- After USS, a forward roll technique is used. Excessive force must not be used. After attempt, CTG is performed and anti-D given if the mother is Rhesus negative. Terbutaline is also given.

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283
Q

What is the efficacy of external cephalic version?

A

The success rate is 50%

spontaneous reversion to breech following this is 3%

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284
Q

What makes external cephalic version difficult?

A
  • Nulliparity
  • difficulty palpating the head
  • high uterine tone
  • an engaged breech
  • less amniotic fluid
  • white ethnicity
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285
Q

What are the absolute contraindications for external cephalic version?

A
  • Caesarean delivery already indicated
  • Antepartum hemorrhage
  • Fetal compromise
  • Oligohydramnios
  • Rhesus isoimmunization
  • Pre-eclampsia
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286
Q

What are the relative contraindications for external cephalic version?

A
  • One previous CS
  • Fetal abnormality
  • Maternal hypertension
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287
Q

What can facilitate external cephalic versions?

A
  • Tocolysis (suppression of uterine contractions) e.g. salbutamol which is given electively or after the first attempt fails
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288
Q

What are the associated risks/ complications of external cephalic versions?

A
  1. pain
  2. precipitation of labour
  3. placental abruption
  4. fetomaternal haemorrhage
  5. cord accidents
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289
Q

What is the most recommended mode of delivery for a breech presentation in labour?

A

CAESAREAN SECTION

however in advanced labour, second twin, preterm, or based on mother’s wishes, vaginal delivery may be more appropriate.

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290
Q

What does TRANSVERSE or OBLIQUE lie mean in labour?

A
  • These types of lie occur when the axis of the fetus is across the axis of the uterus.
  • This is common before term, but only occurs in 1% of fetuses after 37 weeks.
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291
Q

What is an UNSTABLE lie in labour?

A
This occurs when the lie is still changing, usually several  times a day.
Therefore may be:
TRANSVERSE or LONGITUDINAL lie
AND
CEPHALIC or BREECH presentation
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292
Q

How is the ‘lie’ of the fetus assessed?

A
  • Ascertain stability from history: has the presentation been changing?
  • Ascertain fetal like by palpation
  • Neither the head nor the buttocks will be presenting
  • Assess laxity of the uterine wall
  • Does the presenting part move easily?
  • Ultrasound should be performed to help ascertain the cause
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293
Q

What are the risks of abnormal lies?

A
  • Non-longitudinal lie may lead to OBSTRUCTED LABOUR and potential UTERINE RUPTURE
  • Cord prolapse (20%) because with longitudinal lie, the presenting part usually prevents descent of the cord through the cervix.
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294
Q

What is the management for an abnormal lie in labour?

A
  • Admission to hospital from 37 weeks is usually recommended with unstable lie
  • Whilst the lie remains unstable the woman should remain in hospital
  • If the lie does not stabilize, a CS is performed at 41 weeks
  • If the lie is stable but not longitudinal, a CS should be considered at 39 weeks.
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295
Q

What is considered for the mother in twin delivery?

A
  • Twins are induced at 38 weeks gestation but many will have delivered before then.
  • Mum should have IV access and G+S (group and save)
  • Deliver twins in theatre- more space available and immediate surgical intervention if required.
  • Consider epidural
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296
Q

What is considered for the babies in twin delivery?

A
  • Continuous CTG especially in baby 2
  • Monitor lead twin with a fetal scalp electrode and the other abdominally
  • Leading twin should be delivered as for a singleton
  • After delivery of first baby, the lie of the second twin should be checked and stabilized by abdominal palpation, while VE is performed to assess the station of the presenting part.
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297
Q

What are the risks during labour for twin delivery?

A
  • MALPRESENTATION
  • FETAL HYPOXIA in baby 2
  • CORD PROLAPSE
  • OPERATIVE DELIVERY
  • POSTPARTUM HAEMORRHAGE

rarely:

  • CORD ENTANGLEMENT (MCMA twins only)
  • HEAD ENTRAPMENT
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298
Q

What can occur between delivery of first and second baby in twin delivery?

A
  • second twin is usually delivered within 20 mins of the first
  • contractions may diminish after birth of first baby, therefore oxytocin may help
  • If there is distress in baby 2, consider instrumental (forceps/ ventouse) delivery.
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299
Q

How can operative delivery be avoided?

A
  • Encourage continuous support in labour
  • appropriate use of the partogram
  • use of upright/ lateral positions
  • avoid epidural anesthesia/use low-dose epidural
  • appropriate use of oxytocin and delayed pushing in primiparous women with epidurals.
  • delayed pushing with an epidural when the head is in the perineal phase
300
Q

What are the benefits of instrumental vaginal delivery?

A
  • Avoids maternal and perinatal morbidity and mortality

- Avoids an emergency CS

301
Q

What are the maternal indications for instrumental delivery?

A
  • Exhaustion
  • To avoid raising ICP
  • To avoid raising BP
  • Prolonged 2nd stage of labour
  • > 1 hour of active pushing in multiparous woman
  • > 2 hours of active pushing in primiparous woman
  • Medical indications for avoiding Valsalva manouevre such as: severe cardiac disease, hypertensive crisis, uncorrected cerebra vascular malformations.
  • Pushing is not possible (paraplegia/ tetraplegia)
302
Q

What are the fetal indications of instrumental delivery?

A
  • Fetal compromise

- To control the after coming head of breech (forceps)

303
Q

Forceps used in instrumental delivery

A
  • Curved blades which sit around the fetal head and allow traction to be applied- speed up the delivery
  • May be used to slow the rate of the head in a breech delivery
304
Q

What are the three types of forceps used in instrumental delivery?

A
  1. WRIGLEY’S (Low cavity forceps)
  2. NEVILLE BARNES, HAIG FERGUSON, SIMPSON’S)
  3. KEILLAND’S
305
Q

What are Wrigley’s forceps?

A
  • They are low cavity forceps
  • short and light
  • used in CS
306
Q

What are Neville Barnes/ Haig Ferguson/ Simpson’s forceps?

A
  • Midcavity non-rotational forceps
  • “normal”
  • malpresentation can be corrected manually between contractions
307
Q

What are Keilland’s forceps?

A
  • Midcavity rotational forceps
  • reduced pelvic curve on the blades of the forceps allows rotation about the axis of the handle
  • corrects asynclitism and malposition
  • Must only be attempted by a senior operator (or under the close supervision of one)
308
Q

What is ‘ventouse/suction’?

A

Vacuum extractor which uses negative pressure to allow fetal scalp tissues to be sucked in.
It should not be used at <34 weeks gestation

309
Q

What are the three types of ventouse?

A
  1. METAL CUP
  2. SOFT CUP
  3. KIWI OMNI CUP
310
Q

How does the metal cup work in instrumental delivery?

A
  • pressure is created by a suction pump

- excessive traction is likely to cause fetal trauma

311
Q

How does the soft cup work in instrumental delivery?

A
  • softer and easier to apply or OA positions
  • moulds around the fetal head covering a greater surface area
  • causes fewer scalp abrasions
312
Q

How does the Kiwi Omni cup work?

A
  • single use cup
  • pressure created with hand pump (therefore it is quick in emergency
  • allows application to flexion joint in occipitolateral and posterior position
313
Q

What are the requirements for instrumental delivery?

A

FORCEPS

F- Fully dilated cervix
O- OA position preferably, OP is possible with Keilland’s and vacuum
R- Ruptured membranes
C- Cephalic presentation
E- Engaged in presenting part- i.e. the greater diameter of the baby’s head has passed the pelvic brim
P- Pain relief is adequate
— in vacuum extraction or low forceps- minimum of perineal nerve block
— mid forceps- epidural or pudendal nerve block, or GA
S- Sphincter (bladder) empty

314
Q

What are some alternatives to instrumental delivery?

A
  • Encouragement
  • Correct dehydration
  • Increase the uterine contraction
  • C section
315
Q

What are the complications associated with vacuum assisted birth?

A
  • Fetal scalp lacerations and avulsions
  • Cephalhaematoma
  • Retinal haemorrhage
  • Subgaleal haemorrhage (very rare)
316
Q

What are the complications associated with forceps assisted birth?

A

MATERNAL TRAUMA

  • anal sphincter trauma
  • spiral tears of the vagina

FETAL TRAUMA

  • facial nerve palsy
  • skull fractures
  • orbital injury
  • intracranial haemorrhage
317
Q

What is the bottom line in terms of safety of instrumental delivery?

A

VENTOUSE SAFER FOR MOTHER

FORCEPS SAFER FOR BABY

318
Q

When would you abandon instrumental delivery and opt for emergency Caesarean?

A
  • No evidence of progressive descent with each pull (with ventouse, do not mistake increasing caput for descent of the head)
  • Where delivery is not imminent following 3 pulls of a correctly applied instrument by an experienced operator
  • If ‘unsure’ that the instrument will be unsuccessful- try in theatre so that CS can occur if necessary.
319
Q

What are the main indications for a Caesarean Section?

A
  1. Repeat CS
  2. Fetal compromise
  3. Failure to progress in labour
  4. Breech presentation

Maternal request counts for 7% but is not an indication outright.

320
Q

What are the rates of CS?

A

Nulliparous- 24%
Multiparous with no previous CS- <5%
Multiparous with previous CS- 67%

321
Q

What are the risks of caesarean section?

A
  • Abdominal pain
  • VTE
  • Bladder or ureteric injury
  • Hysterectomy
  • Very rarely- maternal death
322
Q

What are the benefits of caesarean section?

A
  • Decreased perineal pain
  • Decreased urinary incontinence
  • Decreased uterovaginal prolapse
323
Q

What are the various timing categories for having CS?

A
  1. IMMEDIATE THREAT TO WOMAN/FETUS
  2. URGENT (but not immediate) MATERNAL/FETAL COMPROMISE
  3. SCHEDULED- no maternal/fetal compromise but needs early delivery
  4. ELECTIVE- delivery timed to suit the woman and staff
324
Q

What are the indications for an immediate threat CS?

A
  • Placental abruption with abnormal FHR or uterine irritability
  • Cord prolapse
  • Scar rupture
  • Prolonged bradycardia
  • scalp pH <7.20
325
Q

What are the indications for urgent CS?

A
  • failure to progress with pathological CTG
326
Q

What are the indications for scheduled CS?

A
  • severe pre-eclampsia
  • IUGR with poor fetal functions test
  • failed induction of labour
327
Q

What are the indications for an elective CS?

A
  • twin pregnancy with non-cephalic first twin
  • maternal HIV
  • Primary genital herpes in the 3rd trimester
  • Placenta praevia
  • Previous hysterectomy or classical CS

electives are usually carried out at 39 weeks, as risk of respiratory morbidity is increased at lower gestational age

328
Q

What are the intraoperative complications of a Caesarean section?

A
  • Uterine lacerations
  • uterocervical lacertions (risk factors for this include low station of presenting part and full dilation, birth weight >4KG, increased maternal age)
  • blood loss (risk factors for this include placenta praevia/abruption, BMI >25 and extremes of fetal birth weight
  • bladder laceration
  • blood transfusion
  • hysterectomy
  • bowel lacerations
329
Q

What are the postoperative complications of a Caesarean section?

A
  • Endometritis
  • Wound infections
  • pulmonary atelectasis
  • venous thromboembolism
  • urinary tract infections
330
Q

What are the risk factors for wound infection post CS?

A
  • preoperative remote infection
  • chorioamnionitis
  • maternal severe systemic disease
  • pre-eclampsia
  • high BMI
  • nulliparity
  • increased surgical blood loss
331
Q

What are the long term complications of a Caesarean section?

A

In subsequent pregnancies:

  • Uterine rupture in subsequent pregnancies
  • placenta praevia
  • placenta accrete
  • antepartum stillbirth

Women undergoing multiple CS are at higher risk of:

  • excessive blood loss
  • difficult delivery of the neonate
  • dense adhesions
  • the risk of any major complication is higher
332
Q

What is shoulder dystocia?

A

Usually when the ANTERIOR SHOULDER is impacted against the SYMPHYSIS PUBIS often due to the failure of INTERNAL ROTATION of the shoulders.

Rarely the posterior shoulder may be impacted against the sacral promontory- causing bilateral impaction

333
Q

What are the fetal complications of shoulder dystocia?

A
  1. Hypoxia and neurological injury
  2. Brachial plexus palsy (Erbs)
  3. Fracture of the clavicle or humerus
  4. Intracranial haemorrhage
  5. Cervical spine injury
  6. Fetal death
334
Q

What are the maternal complications of shoulder dystocia?

A
  1. PPH

2. Genital tract trauma including 3rd + 4th degree perineal tears

335
Q

What are the antenatal risk factors of shoulder dystocia?

A
  • previous history of shoulder dystocia
  • fetal macrosomia
  • BMI >30 and excessive weight gain in pregnancy
  • DM
  • post term pregnancy
336
Q

What are the intrapartum risk factors of shoulder dystocia?

A
  • Lack of progress in late first stage labour
  • induction of labour
  • prolonged second stage
  • instrumental vaginal delivery
  • oxytocin augmentation of labour
337
Q

What is the management for shoulder dystocia?

A
  1. Facilitate the entry of the anterior (or posterior) shoulder into the pelvis
  2. Ensure rotation of the shoulders to the larger oblique or transverse diameter of the pelvis
  3. HELPERR
338
Q

What does HELPERR stand for in the management of shoulder dystocia?

A

H- Help- call for help- additional midwife, senior OB, neonatologist, anesthetist
E- Episiotomy- although shoulder dystocia is a bony problem- this may help with internal maneuvers
L- Legs into McRobert’s (hyper flexed at the hips with thighs abducted and externally rotated)
P- Pressure- suprapubic pressure to dislodge the shoulder from under the symphysis pubis.
E- Enter pelvis for internal maneuvers
R- Release of posterior arm by sweeping the fetal arm across the chest and face
R- Roll over to all fours- this may help delivery by the changes brought about in the pelvis dimensions (Gaskin manoeuvres

339
Q

How do you gain consent for an instrumental delivery?

A
  • Explain that it is not always successful
  • Multiple attempts may be made
  • where delivery is imminent- following 3 pulls of a correctly applied instrument, go to CS
  • could wait to see if labour progresses normally but evidence suggests that fetal life may be compromised
  • explain that all attempts will be made to preserve fetal life but ultimately maternal health is the primary concern
340
Q

What are the signs and symptoms for pre-term labour?

A
  1. CERVICAL WEAKNESS- increased vaginal discharge, mild lower abdominal pain and bulging membranes on examination
  2. INFECTION, INFLAMMATION, ABRUPTION- lower abdominal pain, painful uterine contractions and vaginal loss
341
Q

What are the risk factors for pre-term labour?

A
  • Previous pre-term births
  • multiple pregnancy
  • cervical surgery
  • uterine anomalies
  • medical conditions e.g. renal disease
  • pre-eclampsia and IUGR
342
Q

What is asked in a history in pre-term labour?

A
  • Contractions- onset, frequency, duration, severity
  • constant pain
  • vaginal loss
  • fetal movements
  • obstetric history
343
Q

What would be done on examination in pre-term labour?

A
  • Maternal pulse, temperature, RR (obs)
  • uterine tenderness
  • fetal presentation
  • speculum: look for blood, discharge, liquor
  • swabs (HVS, LVS/perianal)
  • gentle VE
344
Q

What investigations are done in pre-term labour?

A
  • FBC, CRP (raised WCC, and CRP may suggest infection)
  • Swabs, MSU
  • USS for fetal presentation (malpresentation common) and EFW
  • Consider fetal fibronectin/transvaginal USS
345
Q

What is fetal fibronectin?

A

FFN is a protein NOT usually present in cervicovaginal secretions at 22-36 weeks
Those with positive FFN are more likely to deliver (test with swab)
Predicts pre-term birth within 7-10 days of testing

346
Q

What is the management for pre-term labour?

A
  • First, establish whether threatened or ‘real’ pre-term labour, by doing a transvaginal cervical length scan (>15mm unlikely) and FFN assay (is negative, unlikely)
  • Inform SCBU
  • Check fetal presentation with USS
  • Steroids (12mg betametasone IM- two doses 24 hours apart) this will reduce rates of respiratory distress, IVH and neonatal death)
  • Consider tocolysis (nifedipine and atosiban IV to prevent labour and delivery) - this allows time for steroid administration and in-utero transfer
  • Liaison with senior Ops and neonatologists is essential
  • clear plan about: mode of deliver, monitoring in labour, presence of pediatrician
  • give IV antibiotics in labour
347
Q

What is an obstetric emergency?

A

A situation where there is sudden collapse of the patient either antenatally to in the first 6 weeks postpartum. The maternal mortality rate is very low but over 50% of deaths are associated with a poor standard of care.

348
Q

What is the initial approach for an obstetric emergency?

A

Call for help and ABCDEF

A- AIRWAY (recovery position rather than head tilt chin lift due to weight of the baby)
B- BREATHING (RR, sats, auscultate)
C- CIRCULATION- HR, BP, IV access (FBC, U+Es, CRP, crossmatch or G+S), fluid challenges, ABG
D- AVPU, glucose
E- EXAMINATION
F- FETUS, CTG

349
Q

What are the common causes of an emergency?

A
  • antepartum or post partum haemorrhage
  • PE
  • eclampsia
  • myocardial infarction (uncommon but increasing due to increased maternal age)
  • uterine rupture
  • septic shock
  • amniotic fluid embolus
350
Q

What is uterine inversion?

A

It occurs when the placenta fails to detach from the uterus as it exists, pulls on the inside surface and turns the organ inside out- funds inverts into the uterine cavity.

It is associated with grand multis and incorrect management of the third stage

351
Q

What are the signs and symptoms of uterine inversion?

A
  • presents as PPH
  • vaso-vagal shock
  • –> pale
  • –> clammy
  • –> hypotensive
  • –>bradycardic
  • mass at the introitus
  • significant haemorrhage, clotting abnormalities and renal dysfunction can occur if not corrected promptly
352
Q

What is the management for uterine inversion?

A
  • Shock corrects itself when uterus is replaced
  • CAUTIOUS administration of tocolysis to allow uterine relaxation, (although this may aggravate haemorrhage)
  • -> Nitroglycerin (0.25-0.5mg) intravenously over 2mins
  • -> Terbutaline 0.1-0.25mg slowly intravenously
  • -> MgSO4 4-6g intravenously over 20mins
  • Attempting prompt repositioning of the uterus. This is best done manually and quickly, as delay can render repositioning more difficult.
  • Hypotension and hypovolemia require aggressive fluid and blood replacement
  • General anaesthetic or uterine relaxant is then stopped and replaced with oxytocin, ergometrine or prostaglandins.
  • Antibiotics are started and the stimulant continued for at least 24hrs
353
Q

How is manual repositioning of the uterus achieved?

A
  • Reposition the uterus with the placenta if still attached
  • Do this by slowly and steadily pushing upwards towards the umbilicus
  • Maintain bimanual uterine compression and massage until the uterus is well contracted and bleeding has stopped
  • if this fails- O-Sullivan;s method- reduce inversion by hydrostatic technique
354
Q

What are the features of septic shock in pregnancy?

A
  • Antenatally can be any maternal bacterial or viral illness which progresses rapidly e.g. swine flu
  • Severe sepsis can result from mid-trimester rupture of the membranes managed conservatively
  • Postnatally most common organism is Strep A
355
Q

What is the management of septic shock in pregnancy?

A
  • Intravenous brad spectrum antibiotics e.g. cefotaxime, metronidazole +/- gentamicin
  • uterine evacuation later if retained products of conception
356
Q

What is an amniotic fluid embolus?

A

Amniotic fluid, fetal cells, hair or other debris enters the mother’s bloodstream via the placental bed of the uterus and triggers an allergic-like reaction.

357
Q

What are the signs and symptoms of amniotic fluid embolus?

A
  • collapse
  • DIC disseminated intravascular coagulation
  • unaccountable bleeding
  • seizures
  • right heart sided failure
  • ARDS
  • hypotension
358
Q

What is the management for amniotic fluid embolus?

A
  • supportive treatment- ABCDEF incl. blood transfusion, fluid resus
  • early transfer to ITU (as likely to need renal and inotropic support)
  • correct clotting
359
Q

What are the features of uterine rupture?

A
  • rare in primigravida patients
  • almost always occurs in labour
  • 87% of cases occur in women who have had a previous CS
  • high risk in multiparous women on uterine stimulants e.g. oxytocin
360
Q

What are the signs and symptoms of uterine rupture?

A
  • clinically significant uterine bleeding
  • chest or shoulder tip pain and sudden shortness of breath
  • scar pain and tenderness
  • cessation of previously efficient uterine contractions
  • fetal distress
  • protrusion or expulsion of the fetus/ placenta into the abdominal cavity
  • fresh vaginal bleeding
  • haematuria
  • constant, severe abdominal pain which breaks through epidural
  • shock
361
Q

What is the management for uterine rupture?

A
  • ABC including transfusion bloods
  • IV access and basic resuscitation including blood
    immediate laparotomy to salvage baby, repair damage or hysterectomy
362
Q

What is the prognosis for uterine rupture?

A
  • 6.2% of uterine ruptures are associated with perinatal death
  • 14-33% of women with rupture require a hysterectomy
  • if a uterine repair has been achieved it is important to note that repeat rupture occurs in approx. 20% of cases
363
Q

How can uterine rupture be prevented?

A

Cautious use of oxytocin in VBAC

364
Q

What is antepartum haemorrhage?

A
  • Bleeding from the genital tract in pregnancy at >24wks gestation before onset of labour
  • if before 24 weeks: threatened miscarriage
  • anything over 50mls
365
Q

What are the causes of antepartum haemorrhage?

A

97% UNEXPLAINED
( usually marginal placental bleeds)

  • PLACENTA PRAEVIA
  • PLACENTAL ABRUPTION
  • OTHER
  • -> local infection of the cervix/vagina
  • -> a ‘show’- loss of mucus plug
  • -> genital tract tumours
  • -> varicosities
  • -> trauma
  • -> vasa previa
366
Q

What should be considered in the history for antepartum haemorrhage?

A
  • Gestational age
  • amount of bleeding
  • associated to initiating factors
  • abdominal pain
  • fetal movements
  • date of last smear
  • previous episodes of PV bleeding in this pregnancy
  • leakage of fluid PV
  • previous uterine surgery
  • smoking and use of illegal drugs
  • blood group and rhesus status
  • previous obstetric history (placental abruption, IUGR, placenta praevia)
  • position of placenta
367
Q

What is done during maternal assessment in antepartum haemorrhage?

A
  • Blood pressure
  • pulse
  • uterine palpation for size, tenderness, fetal lie, presenting part
  • once placental praevia is excluded, speculum examination to assess degree of bleeding, possible local causes of bleeding and to determine if membranes are ruptured.
368
Q

What is done during fetal assessment in antepartum haemorrhage?

A
  • Can a fetal heart be heard?
  • Ensure that it is fetal and not maternal
  • If fetal heart is hard and gestation is estimated to be 26 weeks to more, FHR monitoring should be commenced
369
Q

What are the two main outcomes of initial assessment?

A
  • BLEEDING IS HEAVY AND CONTINUING- mother and fetus are, or soon will be compromised- therefore treat as massive obstetric haemorrhage

OR

  • BLEEDING IS MINOR AND SETTLING- neither mother or fetus compromised, keep in hospital and watch for 24 hours to make sure it doesn’t progress.
370
Q

What is the maternal management for antepartum haemorrhage?

A
  • Anti D: in the event of APH, all RhD negative women require 500IU of anti-D immunoglobulin, unless they are already sensitized. More anti-D may be required based on the result of the Kelihauer test.
  • Group and save
  • Coagulation screen
  • Cannulate if suspecting large haemorrhage
371
Q

What is the fetal management for antepartum haemorrhage?

A
  • USS for fetal well-being and to confirm placental location
  • Umbilical artery doppler measurement
  • ongoing antenatal management after a limited APH
  • extra surveillance of fetal growth and well-being after discharge.
372
Q

What is Placenta Praevia?

A

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

373
Q

What are the risk factors for placenta praevia?

A
  • previous history of placenta praevia
  • previous caesarean section
  • relative risk after CS increases with multiple CS
  • advancing maternal age
  • increasing parity
  • smoking
  • cocaine use during pregnancy
  • previous spontaneous or induced abortion
  • deficient endometrium due to past history
  • assisted conception
374
Q

What are the main presentations of placental praevia?

A
  • incidental finding on routine anomaly ultrasound
  • painless bleeding starting after the 28th week (typically it is sudden and profuse but usually does not last for long and so is only rarely life-threatening
  • In 15% of cases, the fetus presents in oblique or transverse lie.
  • Can be found early during the 20 week scan
  • -> may be low at scan, but can migrate during 2nd and 3rd trimesters- due to development of the lower uterine segment
375
Q

What is a major (grade III/IV) placenta praevia?

A
  • the placenta lies over the cervical os

- cervical effacement and dilatation would result in catastrophic bleeding and potential maternal and fetal death

376
Q

What is a minor (grade I/II) placenta praevia?

A
  • the placenta lies in the lower segment, close to or encroaching on the cervical os.
377
Q

What is the incidence of placenta praevia?

A

0.5% of pregnancies at term

378
Q

How is placenta praevia diagnosed?

A

Transvaginal USS is safe and more accurate than trans abdominal USS

379
Q

What is the management for placenta praevia?

A
  • women with major PP who have previously bled should be admitted from 34 wks gestation
  • women with asymptomatic PP may remain at home if:
  • -> close to hospital
  • -> aware of risks
  • -> have constant companion
  • -> have communication and transport

Delivery is likely to be CS is placental edge is <2cm from the internal os.

380
Q

What are the complications of placenta praevia?

A
  • Fatal hypovolemic shock resulting from antepartum, intrapartum or postpartum bleeding
  • VTE is associated with prolonged in-patient care, prophylactic anticoagulation is a high risk
  • placenta accreta
  • fetal haemorrhage, prematurity, intrauterine asphyxia or birth injury.
381
Q

What is placenta accreta?

A

Where the placenta is too deeply attached to the uterine wall.

382
Q

What are the varying degrees of placenta accreta?

A

Accreta- Too deeply attached to the uterus
Increta- More deeply attached to the muscle wall of the uterus
Percreta- The placenta grows through the uterus and can extend to nearby organs

383
Q

What is the incidence of placenta accreta?

A

1/2500

384
Q

What are the risk factors for placenta accreta?

A
  • previous caesarean section
  • placenta praevia
  • advanced maternal age
385
Q

What is placental abruption?

A

When the placenta separates from the uterus before delivery of the fetus. Blood accumulates behind the placenta in the uterine cavity or is lost through the cervix.

386
Q

What is the incidence of placental abruption?

A

0.5-1% of pregnancies

387
Q

What are the two main types of placental abruption?

A
  1. CONCEALED

2. REVEALED

388
Q

What is concealed placental abruption?

A
  • No external bleeding evident
  • haemorrhage is confined within the uterine cavity
  • this is the most severe form, as the amount of blood loss is easily underestimated
389
Q

What is revealed placental abruption?

A
  • vaginal bleeding
  • blood drains through the cervix
  • usually with incomplete placental detachment and fewer associated problems
390
Q

What are the risk factors associated with placental abruption?

A
  • previous abruption
  • multiple pregnancy
  • trauma: RTA, domestic violence
  • iatrogenic e.g. external cephalic version
  • threatened miscarriage
  • pre-eclampsia
  • hypertension
  • multiparity
  • previous CS
  • non-vertex presentations
  • smoking
  • cocaine/ amphetamine use
  • thrombophilia
  • intrauterine infections
  • polyhydramnios
391
Q

What are the signs and symptoms of placental abruption?

A
  • abdominal pain (sudden onset, severe, constant)
  • posterior placentas may give rise to severe backache
  • uterus tender on palpation
  • uterine activity is common
  • uterus may later become hard “woody”
  • many will be in labour
  • variable bleeding (often dark)
  • maternal hypovolemia
  • maternal signs of shock
  • fetal distress
392
Q

How is the diagnosis for placental abruption made?

A

CLINICAL DIAGNOSIS

  • USS is only used to confirm fetal well-being and exclude placenta praevia
  • fetal hypoxia due to an abruption will lead to heart rate abnormalities on CTG
  • low platelet count may signify abruption
  • maternal collapse and potential fetal death

BP MAY BE NORMAL!

393
Q

What is the management for placental abruption?

A

Admit all women with vaginal bleeding or unexplained abdominal pain

  • Establish immediate fetal well-being with CTG and USS
  • if fetal distress/ maternal compromise, resuscitate and deliver- ABCDEF
  • If no fetal distress and bleeding and pain cease, consider delivering at term.
394
Q

What is the puerperium?

A

The 6 week period of time after delivery of the placenta until the reproductive organs have returned to their pre-pregnant state.

395
Q

What happens to the hormones post-partum?

A
  • Human placental lactose and bhCG: levels fall rapidly and by 10 days neither should be detectable.
  • Oestrogen and progesterone: non-pregnancy levels are achieved by 7 days post-partum.
396
Q

What happens to the uterus postpartum?

A
  • Rapid involution, the weight of the uterus falls from 1kg post delivery to 500g at the end of a week.
  • By two weeks the uterus should return to the pelvis and no longer be palpable abdominally.
397
Q

What happens to the vagina postpartum?

A
  • The vaginal wall is swollen initially, but rapidly regains tone
  • Gradually vascularity and oedema decrease
398
Q

What happens to the cervix postpartum?

A
  • The cervical os gradually closes after delivery

- It admits 2-3 fingers for the first 4-6 days and by the end of days 10-14, is is dilated to around 1cm

399
Q

What happens to the perineum postpartum?

A

Perineal oedema may persist for some days. It may take longer in women who had perineal tears that needed repair.

400
Q

What is lochia?

A

Lochia constitutes of sloughed-off necrotic decidual layer mixed with blood. It is initially red (lochia rubra), becomes paler as the bleeding is reduced (lochia serosa) and finally becomes a yellowish white (lochia alba).

The flow of lochia may last for 3-6 weeks.

401
Q

What is important to remember in post-natal care?

A
  • Maternal observations
  • pain relief (for perineal trauma, or LSCS wound)
  • observe lochia and involution
  • observe wounds
  • ensure urine is passed normally
  • eating and drinking/ flatus and stool
  • VTE risk assessment
  • encourage mobility to prevent VTE
  • observe for signs of VTE
  • HB check if signs of anaemia
  • Rubella vaccination MMR
  • Anti D for rhesus negative women
  • early neonatal feeding/ neonatal care
402
Q

What happens to the breasts postpartum?

A

Between the 2nd and 4th days, the breasts become engorged, the vascularity is increased and areola pigmentation increases.
There is enlargement of the lobules resulting from an increase in the number and size of the alveoli

403
Q

What happens to the cardiovascular system postpartum?

A
  • Cardiac output initially increases then rapidly decreases to about 40% of the pre-labour levels as a result of diuresis.
  • It returns to normal by 2-3 weeks postpartum.
  • Heart rate also decreases and is partly responsible for decreased cardiac output
  • Blood loss at delivery and excretion of extracellular fluid are responsible for alterations in the blood volume.
404
Q

What is an episiotomy?

A

A surgical incision to enlarge the vaginal introitus and facilitate childbirth

405
Q

What are the two main types of episiotomy?

A
  • MEDIOLATERAL EPISIOTOMY- extends from the fourchette laterally (thus reducing the risk of anal sphincter injury)
  • MIDLINE EPISIOTOMY- extends from the fourchette towards the anus
406
Q

What are the indications for an episiotomy?

A
  1. Complicated Vaginal Delivery
    - - breech
    - - shoulder dystocia
    - - forceps
    - - ventouse
  2. Extensive lower genital tract scarring
    - - female genital mutilation
    - - poorly healed 3rd/4th degree tears
  3. Fetal Distress
407
Q

What are the general complications of perineal trauma?

A
  • Bleeding
  • haematoma
  • pain
  • infection
  • scarring with potential disruption to the anatomy
  • dyspareunia
  • fistula formation
408
Q

What are the classifications of perineal tears?

A

1ST DEGREE- injury to the skin only

2ND DEGREE- injury to the perineum involving perineal muscle (includes episiotomy)

3RD DEGREE- injury to the perineum involving the anal sphincter complex:
3a- <50% of the external anal sphincter thickness torn
3b- >50% of the external anal sphincter thickness torn
3c- internal anal sphincter torn

4TH DEGREE- injury to the perineum involving the anal sphincter couples (EAS and IAS) and the anal/rectal epithelium.

409
Q

What are the risk factors for anal sphincter trauma?

A
  • forceps delivery
  • nulliparity
  • shoulder dystocia
  • 2nd stage >1 hour
  • persistent OP position
  • midline episiotomy
  • birth weight >4kg
  • epidural anaesthesia
  • induction of labour
410
Q

What is the management for perineal tear?

A

SURGICAL REPAIR

  • suture ASAP to reduce bleeding and infection risk
  • PR before to ensure no AS involvement
  • repair in theatre
  • lithotomy position
  • consider cosmetic results
  • PR following to ensure no suture has passed into rectum
  • count needles and swabs
411
Q

What are the management considerations for 3rd and 4th degree tears?

A
  • anal sphincter laceration is associated with anal incontinence.
  • women must receive broad spectrum antibiotics and stool softeners
  • they should receive physiotherapy input
  • follow up at 6-12 weeks is also important
412
Q

What are the three major causes of morbidity in the postnatal period?

A
  1. SECONDARY POSTPARTUM HAEMORRHAGE (PPH)
  2. VTE
  3. PUERPURAL PYREXIA/FEVER
413
Q

What is primary PPH?

A

Blood loss of 500ml or more from the genital tract occurring within 24 hours of delivery

414
Q

What is secondary PPH?

A

Excessive loss occurring between 24hrs and 6 weeks after delivery

415
Q

What are the risk factors for PPH?

A

TONE- uterine atony (90%): failure of the uterus to contract after delivery
TRAUMA- tears, episiotomy, lacerations of the cervix and rupture of the uterus
TISSUE- retained placenta
THROMBIN- coagulopathy: severe pre-eclampsia, placental abruption and sepsis.

Also:

  • large placenta
  • abnormal placental site (placenta praevia, placenta accreta)
  • uterine inversion
416
Q

What are the antenatal risk factors for PPH?

A
  • previous PPH
  • previous retained placenta
  • maternal H of <8.5g/dL at onset of labour
  • increased BMI
  • para >4
  • APH
  • overdistension of the uterus (multip/polyhydramnios)
  • uterine abnormalities
  • low lying placenta
  • maternal age >35
417
Q

What are the intrapartum risks of PPH?

A
  • induction of labour
  • prolonged labour at 1st, 2nd or 3rd stage
  • use of oxytocin
  • precipitate labour
  • vaginal operative delivery
  • CS
418
Q

Who to contact in management for minor PPH (500-1000ml lost)

A
  • midwife in charge

- first line obstetric and anaesthetic staff

419
Q

Who to contact in management for major PPH (>1000ml)

A
  • experienced midwife as well as midwife in charge
  • obstetric middle grade and alert consultant
  • anesthetic middle grade and alert consultant
  • alert consultant clinical hematologist on call
  • alert blood transfusion laboratory
  • call porters for delivery of blood/specimen
  • one member of the team to record events fluids, drugs and vital signs
420
Q

How to manage major PPH?

A

Three main principles:

  1. empty uterus (fetus or tissue)
  2. treat uterine atony (physically, medically, surgically)
  3. repair genital tract trauma.
  • Empty uterus (deliver fetus)
  • remove placenta or retained tissue - active management if still in 3rd stage
  • apply bimanual compression
  • massage uterus (to rub up a contraction)
  • give crystalloid (fluids)
  • give drugs to increase uterine contraction
  • repair any genital tract injuries (including cervical tears)
  • uterine tamponade with a Rusch balloon
  • Lapratomy
  • –> suture over placental bed
  • –> uterine artery embolization may be helpful but is not always an option in emergency situations
  • –> total or subtotal hysterectomy
421
Q

What are the drugs given to increase uterine contraction in the management of PPH?

A
  • Syntocinon 5U by slow intravenous injection- infusion
  • Ergometrine 500 micrograms IV or IM bolus
  • Syntocinon- 40 IU infusion
  • Caroprost 250 micrograms IM injection
  • Misoprostol 800-1000 micrograms PR
422
Q

What is puerperal pyrexia?

A

the presence of fever in a mother >38 degrees in the first 14 days after giving birth

423
Q

What are the antepartum factors predisposing to puerperal pyrexia?

A
  • anaemia

- duration of membrane rupture

424
Q

What are the intrapartum factors predisposing to puerperal pyrexia?

A
  • duration of labour
  • bacterial contamination during vaginal examination
  • instrumentation
  • trauma e.g. episiotomy, vaginal tears, CS
  • haematoma
425
Q

What are the causes of puerperal pyrexia?

A
  1. UTERINE INFECTION
  2. PERINEAL WOUND INFECTION
  3. BREAST CAUSES
  4. UTI
  5. THROMBOPHLEBITIS
  6. RESPIRATORY COMPLICATIONS
  7. ABDOMINAL WOUND INFECTIONS
  8. ORGANISMS
426
Q

Uterine infection cause of puerperal pyrexia

A
  • CS
  • intrapartum chorioamnionitis
  • prolonged labour
  • multiple pelvic examinations
  • internal fetal monitoring

symptoms

  • foul, profuse, bloody discharge
  • subinvolution of uterus
  • tender bulky uterus on abdominal examination
427
Q

Perineal wound infection cause of puerperal pyrexia

A
  • includes infection of episiotomy wounds and repaired lacerations
  • perineum becomes painful
  • breakdown of wound
428
Q

Breast causes of puerperal pyrexia

A
  • About 15% of women develop fever from breast engorgement
  • fever may be up to 39 degrees
  • associated with hard and painful breast
  • may need antibiotics
  • continue breast feeding
  • abscess may need drainage
429
Q

UTI cause of puerperal pyrexia

A
  • 2-4% of women develop UTI postpartum
  • hypotonic bladder may result in stasis and reflux of urine
  • catheterization, birth trauma, and pelvic exam during labour may introduce infection
  • increased frequency, micturition, dysuria, urgency
  • rigors present in pyelonephritis
  • E. coli, proteus, Klebsiella
430
Q

Thrombophlebitis cause of puerperal pyrexia

A
  • Superficial or deep venous thrombosis of leg may cause pyrexia
  • Caused by venous stasis
  • diagnosis made by the observation of a painful, swollen leg, usually accompanied by calf tenderness
  • high risk of postpartum DVT and PE- be vigilant with investigations
431
Q

Respiratory causes of puerperal pyrexia

A
  • usually seen within the first 24 hours after delivery
  • almost invariably in CS
  • complications due to atelectasis, aspiration, and bacterial pneumonia
432
Q

Abdominal wound causes of puerperal pyrexia

A

risk factors include:

  • obesity
  • diabetes
  • corticosteroid therapy
  • poor homeostasis at surgery with subsequent hematoma
433
Q

Organisms responsible in puerperal pyrexia

A
  • Group A strep
  • Staph, Enterococcus (gram +)
  • Anaerobes e.g. peptococcus, peptostreptococcus
434
Q

What investigations are done in puerperal pyrexia?

A
  • Blood cultures
  • MSU
  • swabs from cervix, lochia for chlamydia and bacterial culture
  • wound swabs
  • throat swabs
  • CXR, sputum culture
435
Q

What is the supportive management for puerperal pyrexia?

A
  • Analgesics and NSAIDS
  • wound care in case of wound infection
  • ice packs for pain from perineum or mastitis
436
Q

What is the antibiotic management for puerperal pyrexia?

A
  • Co-amoxiclav or cefuroxime and metronidazole
  • Clindamycin and aminogycoside (e.g. gentamicin) is appropriate for the treatment of endometritis
  • Tetracyclines should be avoided in breast-feeding women
  • Involvement of micro team for those who fail to respond.
437
Q

What is eclampsia?

A

Grand mal convulsions following pre-eclampsia. There his high maternal and perinatal mortality and repeated fits are common

438
Q

How is eclampsia managed?

A
  • ABC
  • Give diazepam and MgSO4 to stop fits
  • prevent further fits by commencing MgSO4 infusion
  • stabilize blood pressure and maternal condition
  • deliver baby
  • always try to control blood pressure and deliver baby before hypertensive crisis- Labetalol is first choice followed by nifedipine
  • No proven value in prophylactic anticonvulsants in pre-eclampsia
439
Q

VTE/PE in pregnancy

A
  • Pregnancy is a pro-thrombotic state, as coagulation factors alter to promote clotting, and there is a large pelvic mass and reduced mobility.
440
Q

What are the signs and symptoms of VTE/PE in pregnancy?

A
  • asymptomatic
  • pleuritic chest pain
  • SOB
  • collapse
  • hypotension
  • tachycardia
  • reduced air entry
  • reduced oxygen saturations
441
Q

What is the management for VTE/ PE in pregnancy

A
  • ABCDEF
  • Facial oxygen
  • ABG, CXR, ECG, V/Q scan
  • if clinically suspicious, anti-coagulate while awaiting results
  • LWMH until 6 months post birth
442
Q

What is colostrum?

A
  • Thick, yellow, fluid produced from around 20 weeks
  • high concentration of secretory IgA
  • rich in protein- helps with gut maturation and immunity for baby
  • produced in small quantities following birth
443
Q

Human milk

A
  • amount of milk produced increases rapidly up to 500ml at 5 days postpartum
  • 57-65kcal/dL
  • exclusively breast fed infants feed 8 times a day- 6 during the day, 2 during the night
  • feeds are sparse and infrequent in the first 24-48 hours, gradually increases and reaches peak at 5th day of life
444
Q

What are the advantages of breast feeding for the baby?

A
  • GI illness- less morbidity from GI infection than mixed feed
  • UTI- natural defense against UTI
  • Respiratory infection- protection in exclusive breast feeding
  • Atopic illness- less likely to have eczema and asthma
  • Leukemias- reduced risk
  • Giardiasis protection if mother is immune
  • Bonding
445
Q

What are the maternal advantages of breast feeding?

A
  • Uterine involution- reduces risk of PPH
  • Amenorrhoea and contraception- lactational amenorrhoea is 97% effective as contraception in full/nearly full breastfeeding
  • Cancer- breastfeeding can protect against premenopausal breast, ovarian cancers and osteoporosis
  • Bonding
  • Cost effective
446
Q

What are potential problems with breastfeeding?

A
  1. INADEQUATE MILK SUPPLY
  2. PROBLEMS WITH MILK FLOW
  3. MASTITIS (non infective and infective)
  4. BREAST ABSCESS
447
Q

What are the treatments for insufficient milk supply?

A
  • adequate fluid
  • nutrition
  • secure and private environment
  • dopamine antagonists
  • thyrotropin-releasing hormone
  • oxytocin
448
Q

What are some of the potential problems with milk flow?

A
  • breast engorgement, mastitis and breast abscess are limitations on feeding frequency and duration
  • There may be problems with positioning the baby- which can be solved by allowing baby unrestricted access to the breast
  • Sore and cracked nipples- may be necessary to rest the breast and express the milk manually until the crack has healed
449
Q

What is non infective mastitis?

A

It results from obstruction of milk drainage from one section of the breast, which may be due to:

  • restriction of feeding
  • badly positioned baby
  • blocked ducts
  • compression from fingers holding the breast or from wearing a small bra
450
Q

How is non-infective mastitis characterized?

A
  • swollen, red, painful breast
  • tachycardia
  • pyrexia
  • aching, flu-like feeling
  • shivering and rigors
451
Q

How is non-infective mastitis resolved?

A

Relieving the obstruction by continuing to breast feed with correct positioning of the baby

452
Q

What is the most common organism involved in infective mastitis?

A

Staphylococcus aureus

453
Q

Which antibiotics should be used in infective mastitis?

A
  • flucloxacillin
  • amoxicillin + clavulanate
  • cefalosporins (cefalexin cefadrine, cefaclor)
454
Q

Postpartum contraception points to consider:

A
  • Contraception is not needed in the first three weeks
455
Q

What are the main types of postpartum contraception?

A
  1. Breast feeding (lactational amenorrhoea method)
  2. Progesterone only pill (POP)
  3. Combined oral contraceptive pill (COCP)
  4. Implants
  5. IUCD and levonorgestrel- releasing IUS
456
Q

How does the breast feeding (lactational amenorrhoea method) work?

A
  • A suckling infant reduces the release of gonadotrophin, which suppress ovulation- however as suckling reduces, ovulation returns.
    It is 98% effective if a woman is
  • less than six months PP
  • amenorrhoeic (no vaginal bleeding after the first 56 days PP)
  • full breast feeding day and night
457
Q

When does the risk of pregnancy increase in the lactational amenorrhoea method?

A
  • breastfeeding decreases, particularly stopping night feeds or with the introduction of formulas or solids
  • menstruation resumes
  • the woman is more than 6 months PP
458
Q

What is the regime for POP as postpartum contraception?

A
  • Commence up to day 21 PP without the need for extra contraception
  • if started after day 21, additional contraception is needed for 2 days and need to exclude pregnancy
  • if regular menstrual cycles have retuned, start POP up to and including day 5 of period without the need for extra barrier methods.
  • breast feeding women can start POP without the need for extra contraceptive methods
459
Q

What should be considered when starting COCP as postpartum contraception?

A

AVOID IN LACTATING WOMEN

  • it can affect milk composition and increase the incidence of breast feeding failure
  • bottle feeding women can start COCP 21 days postpartum
  • If started later than 21 days, additional barrier methods of contraception are needed for 7 days.
  • There may be increased risk of VTE with earlier commencement of COCP
460
Q

Implant as postpartum contraception method:

A
  • Allowed in both breast feeding and non-breast feeding women
  • Start 21-28 days after delivery
  • If later than day 21, extra barrier methods of contraception are needed for 7 days
461
Q

IUCD and levonorgestrel releasing-IUS postpartum contraception method:

A
  • These have no effect on breast milk production
  • 1 in 20 expulsion risk
  • review 4-6 weeks after insertion
  • teach the woman to feel threads after each period
  • may be fitted from 4wks postpartum, Mirena says 6 wks
462
Q

How is postnatal maternal mental illness categorized?

A
  • BABY BLUES- up to 75% of women
  • POSTNATAL DEPRESSION- 10-15% of women
  • PUERPERAL PSYCHOSIS- 1:500 women - significant cause of maternal death!
463
Q

Baby Blues:

A
  • It is characterized by:
  • tearfullness
  • irritability
  • anxiety
  • poor sleep

This usually responds to support and reassurance

464
Q

Postnatal Depression:

A

Key features include:

  • tearfullness
  • irritability
  • anxiety
  • poor sleep
465
Q

What are the treatment and recovery options for those suffering with postnatal depression?

A
  • Milld- moderate depression may respond to self help strategies and non-directive counseling
  • Moderate to severe depression usually requires treatment with antidepressant medication and/or CBT
  • breastfeeding is not a contraindication for antidepressant treatment, but drugs with low excretion in breast milk such as SERTRALINE are preferred
466
Q

What is puerperal psychosis?

A

A range of psychotic conditions presenting in the immediate postnatal period.
It presents rapidly- usually within the first 2 weeks of delivery

467
Q

What are the risk factors for developing puerperal psychosis?

A
  • History of bipolar disorder
  • previous puerperal psychosis
  • 1st degree relative with history of puerperal psychosis
  • 1st degree relative with bipolar affective disorder
468
Q

What are the treatment and recovery for those suffering with puerperal psychosis?

A
  • Urgent psychiatric assessment and treatment
  • admissions- due to risk to both mother and baby- ideally to a specialist mother-baby unit

it is treated according to diagnosis, therefore options also include:

  • antidepressant or antipsychotic medication
  • mood stabilizers
  • ECT

Most make full recovery, but 10-year recurrence rate is up to 80%

469
Q

What constitutes abnormal bleeding?

A

Any menstrual bleeding that is:

  • abnormal in volume (excessive duration or heavy)
  • regularity or timing (delayed or frequent)
  • non-menstrual (IMB, PCB, PMB)
470
Q

Menorrhagia

A

Heavy menstrual bleeding

471
Q

Intermenstrual bleeding (IMB)

A

Bleeding between periods

472
Q

Irregular periods

A

Periods outside the range of 23-25 days with a variability of 7 days between the longest and shortest cycle

473
Q

Postcoital bleeding (PCB)

A

Bleeding after intercourse

474
Q

Primary amenorrhoea

A

Periods never start/ lack of menstruation by age 16

475
Q

Secondary amenorrhoea

A

Periods stop for 6 months or more

476
Q

Oligomenorrhoea

A

Infrequent periods (>every 35 days- 6 months)

477
Q

Postmenopausal bleeding (PMB)

A

Bleeding 1 year after the menopause

478
Q

Dysmenorrhoea

A

Painful periods

479
Q

Premenstrual syndrome

A

Psychological and physical symptoms worse in the luteal phase

480
Q

Primary dysmenorrhoea

A

The pain has no obvious organic cause. Potential causes include:

  • abnormal progesterone ratios or sensitivity
  • neuropathic dysregulation
  • venous pelvic congestion
  • psychological causes
481
Q

Secondary dysmenorrhoea

A

The pain is due to an underlying condition:

  • Endometriosis
  • Adenomyosis
  • Pelvic Inflammatory Disease (PID)
  • Pelvic adhesions
  • Fibroids
  • Cervical stenosis (iatrogenic- post LLETZ [large loop excision of the transitional zone] or instrumentation)
  • Asherman’s syndrome
  • Congenital abnormalities
482
Q

What should be included in a history for dysmenorrhoea?

A
  • Timing and severity of pain (including degree of functional loss)
  • If the pain is premenstrual then eases off (common presentation)
  • Questions about pelvic pain and deep/superficial dyspareunia
  • Previous history of PID or STI
  • Previous abdominal or genital tract surgery
483
Q

What should be done in examination for dysmenorrhoea?

A
  • Abdominal exam to exclude pelvic masses

- Pelvic exam: cervical excitation, adnexal tenderness and masses

484
Q

What investigations should be done for dysmenorrhoea?

A
  • STI screen (including chlamydia swab)
  • TVS (transvaginal sonography): endometriomata, PID sequelae, fibroids, congenital abnormalities
  • Laparoscopy is usually reserved for women with TVS abnormalities, medical treatment failures, or those with concomitant subfertility.
485
Q

What is the conservative management for dysmenorrhea?

A

Appropriate reassurance and analgesia

486
Q

What is the symptomatic control management for dysmenorrhoea?

A
  • mefenamic acid 500mg TDS with each period
  • COCP to abolish ovulation
  • Mirena IUS
  • paracetamol, hot water bottles
487
Q

What is the treatment for underlying causes in dysmenorrhoea?

A
  • endometriosis: COCP, progestogens, GnRH analogues
  • antibiotics for PID
  • relief of obstruction (usually surgical)
488
Q

What is the surgical management for underlying causes in dysmenorrhea?

A

Therapeutic laparoscopy:
- gold standard for diagnosis and management of endometriosis/adhesions/complicated PID

Hysterectomy: now rare for this condition alone

489
Q

What are the main causes for amenorrhoea?

A
  1. Hypothalamic: Functional
  2. Hypothalamic: Non- functional
  3. Anterior pituitary
  4. Ovarian
  5. Genital tract outflow obstruction
  6. Endocrinopathies
  7. Oestrogen/ androgen secreting tumors
490
Q

What are examples of functional hypothalamic causes for amenorrhoea?

A
  • stress
  • anorexia
  • excessive exercise
  • pseudocyesis
491
Q

What are examples of non-functional hypothalamic causes for amenorrhoea?

A
  • SOL
  • surgery
  • radiotherapy
  • Kallman’s syndrome (1st degree GnRH deficiency)
492
Q

What are examples of anterior pituitary causes for amenorrhoea?

A
  • micro/macroadenoma (prolactinoma) or other SOL surgery

- Sheehan’s syndrome (postpartum pituitary failure)

493
Q

What are examples of ovarian causes for amenorrhoea?

A
  • PCOS
  • POF (premature ovarian failure)
  • resistant ovary syndrome
  • ovarian dysgenesis, especially due to Turner’s syndrome
494
Q

What are examples of genital tract outflow obstruction causes for amenorrhoea?

A
  • imperforate hymen
  • transverse vaginal septum
  • cervical stenosis
  • Asherman’s syndrome (iatrogenic intrauterine adhesions)
495
Q

What are examples of endocrine causes for amenorrhoea?

A
  • hyperprolactinaemia
  • Cushing’s syndrome
  • severe hypo/hyperthyroidism
  • CAH (congenital adrenal hyperplasia)
496
Q

What are examples of oestrongenic/androgenic causes for amenorrhoea?

A
  • granulosa- teca cell tumours

- gynadroblastoma

497
Q

What are the investigations for amenorrhoea?

A
  • PREGNANCY TEST
  • FSH/LH (increased in POF), (decreased in hypothalamic causes)
  • TESTOSTERONE AND SHBG
  • PROLACTIN
  • TFTs
  • PELVIC USS
  • -> can define anatomical structures, congenital abnormalities, Asherman’s syndrome, haematometra and PCOS morphology)
  • -> can indicate physiological activity; endometrial atrophy in POF
  • KARYOTYPE- if uterus is absent or suspicion of Turner’s syndrome
  • Specific tests for endocrinopathies in clinical suspicion
498
Q

What are the causes of oligomenorrhea?

A
  • Anvoluntary cycles
  • PCOS- the commonest cause
  • Borderline low BMI
  • Obesity without PCOS
  • Ovarian resistance leading to anovulation
  • milder degrees of hyperprolactinaemia
499
Q

What is the management for oligomenorrhea?

A
  • Provide reassurance
  • Treat any underlying causes as for amenorrhoea
  • attain normal BMI (weight loss/gain as appropriate)
  • provide regular cycles- COCP/ cyclical progestogens
  • in PCOS a minimum of 3 periods/year is recommended to decrease risk of endometrial hyperplasia
  • full fertility screening should be performed
500
Q

What is premenstrual syndrome?

A
  • Distressing psychological, physical and/behavioural symptoms
  • occurs during the luteal phase of the menstrual cycle
  • significant regression of symptoms with onset during the period
  • most women self- diagnose
501
Q

How is moderate-severe PMS diagnosed/characterized?

A

When there is disruption of interpersonal/work relationships, or interference with normal activities.

502
Q

How is severe PMS diagnosed/ characterized?

A

when >5 symptoms are present for most of the late luteal phase with remission within a few days of menses, and absence of symptoms in the week post menses.

The symptoms include at least one:

  • Markedly depressed mood, feelings of hopelessness or self-deprecation
  • Marked anxiety, tension (being on edge)
  • Marked affective lability (feeling suddenly sad/tearful)
  • Persistent and marked anger/ irritability/ increased conflicts

PLUS

  • Decreased interest in usual activities (school, friends, hobbies)
  • Subjective sense of difficulty in concentration
  • Lethargy, easy fatiguability/ lack of energy
  • Marked change in appetite, overeating or specific food cravings
  • Hypersomnia or insomnia
  • subjective sense of being overwhelmed and out of control
  • Other physical symptoms such as beast tenderness or swelling, headaches, joint or muscle pain, a sense of bloating, weight gain.
503
Q

What is the hormonal management for PMS?

A
  • COCP
  • Danazol
  • Oestrogen
  • GnRH analogues +/- add back HRT are of proven benefit for moderate-severe PMS but with a license for 6 month treatment only due to bone loss
504
Q

What is the non-hormonal management for PMS?

A
  • SSRIs, antidepressants
505
Q

What self-help is available for those suffering with PMS?

A
  • dietary alteration (less fat, sugar, salt, caffeine and alcohol
  • Vitamin B6 supplements
  • Magnesium supplements seem most effective for premenstrual anxiety
  • exercise
  • stress reduction/ relaxation techniques
  • healthier lifestyle
  • complementary therapy
506
Q

What is the prevalence of PCOS?

A
  • 6-10% of women of childbearing age

- it is responsible for 80% of all cases of anovulatory subfertility.

507
Q

What are the main causes of PCOS?

A
  1. HYPERSECRETION of LH
  2. GENETIC (familial clustering)
  3. INSULIN RESISTANCE WTH COMPENSATORY HYPERINSULINAEMIA (defect on insulin receptor)
  4. HYPERANDROGENISM (elevated ovarian angroden secretion)
  5. OBESITY
    - -> BMI >30
    - -> central obesity
    - -> worsens insulin resistance
508
Q

What are the investigations for PCOS?

A

EXAMINATION

  • BMI
  • Signs of endocrinopathy/hirsutism/acne/alopecia

BLOODS

  • hyperglycemia
  • hyperlipidemia
  • basal (day 2-5): LH, FSH, TFTs, prolactin, testosterone
  • in hyperandrogenism
  • -> dehydroepiandrosterone sulfate (DHEAS)
  • -> androstenedione
  • -> sex hormone binding globulin (SHBG)

IMAGING
- Pelvic USS

Exclude other causes of secondary amenorrhoea

509
Q

What is the criteria for diagnosing PCOS

A

ROTTERDAM CRITERIA

510
Q

What is the Rotterdam criteria for diagnosing PCOS?

A

2 OUT OF 3…

  1. Irregular or absent ovulations (cycle >42 days)
  2. Clinical or biochemical signs of hyperandrogenism
    - -> acne
    - -> hirsutism
    - -> alopecia
  3. Polycystic ovaries on pelvic USS
    - -> >12 antral follicles on one ovary
    - -> Ovarian volume >10mL
511
Q

What are the long term complications of PCOS?

A
  • Risk factors for ISCHAEMIC HEART DISEASE (obesity, hypelipidaemia)
  • TYPE 2 DIABETES - risk of obesity and insulin resistance, and pregnant women with PCOS are at increased risk of gestational diabetes
  • ENDOMETRIAL HYPERPLASIA/ CARCINOMA- increased risk due to long periods of secondary amenorrhoea with resultant unopposed oestrogen
512
Q

What are the lifestyle management options for PCOS?

A
  • WEIGHT LOSS

- EXERCISE

513
Q

What are the management options for improving menstrual regularity in PCOS?

A
  • Weight loss
  • COCP
  • Metformin
514
Q

What are the management options for controlling symptoms of hyperandrogenism?

A
  • COSMETIC (depilatory cream/ electrolysis/ shaving/ plucking)
  • Anti-androgens, facial cream, finasteride, or spironolactone:
  • –>which works on acne and hirsutism, can take 6-9 months to improve hair growth, but AVOID IN PREGNANCY (feminizes male fetus)

COCP: dianette
–> a regular monthly withdrawal bleed and beneficial anti-androgenic effects

515
Q

What are the management options for subfertility in PCOS?

A
  • Weight loss
  • Ovulation induction with antioestrogens or gonadotrophins
  • Laparoscopic ovarian diathermy
  • IVF **women with PCOS who undergo IVF are at increased risk of ovarian hyperstimulation syndrome
516
Q

What are the management options for insulin sensitizers for PCOS?

A

METFORMIN

517
Q

What are the management options for the psychological issues experienced during PCOS?

A
  • Be aware of psychological effects of PCOS, counsel and advise accordingly.
  • Take a holistic approach
518
Q

Menopause:

A

the permanent cessation of menstruation, the last menstrual period but only diagnosed in retrospect. It is 12 MONTHS PERIOD FREE

519
Q

Perimenopause:

A

Beginning with the first clinical, biological and endocrinological features of the approaching menopause, such as vasomotor symptoms and menstrual irregularity and ends 12 months after the last period.

520
Q

Premenopause:

A

1-2 years immediately before the menopause or to the whole of the reproductive period before the menopause

521
Q

Postmenopause:

A

Should be defined from the final menstrual period regardless of whether the menopause was induced or spontaneous

522
Q

Menopause transition:

A

The period of time before the final menstrual period, when variability in the menstrual cycle usually is increased.

523
Q

What are the symptoms of early menopause?

A
  • VASOMOTOR/ FLUSHING (hot flushes and night sweats)
  • PERIODS CHANGING
  • INSOMNIA (tiredness, irritability, poor concentration)
  • MOOD SWINGS
  • SEXUAL DYSFUNCTION
  • COGNITIVE FUNCTION/ PSYCHOLOGICAL SYMPTOMS
  • CONNECTIVE TISSUE LOSS
  • FAT REDISTRIBUTION
524
Q

What type of sexual dysfunction symptoms present in early menopause?

A
  • loss of sexual desire
  • loss of sexual arousal
  • problems with orgasm
  • sexual pain (painful sex, dyspareunia)
525
Q

What type of psychological symptoms present in early menopause?

A
  • coping mechanisms
  • depressed mood
  • anxiety
  • irritability
  • lethargy and lack of energy
526
Q

What are the symptoms experienced in the medium term of menopause?

A
  • UROGENITAL ATROPHY (oestrogen deficiency after menopause causes atrophic changes within the urogenital tract)
  • VAGINAL ATROPHY (itching, burning, dryness, soreness, dyspareunia)
  • BLADDER SYMPTOMS (frequency, urgency, nocturia, incontinence, dysuria, UTIs)
527
Q

What are some long term risks of menopause?

A
  1. OSTEOPOROSIS

2. CARDIOVASCULAR DISEASE

528
Q

What is the management for menopause?

A
  • EDUCATION ON HEALTHY AGING AND REASSURANCE
  • LIFESTYLE ADJUSTMENTS
  • -> sustained regular exercise
  • -> lighter clothing
  • -> reducing stress
  • -> avoidance of possible triggers e.g. spicy food, caffeine, alcohol
  • HORMONE REPLACEMENT THERAPY
  • there are more than 50 hormone replacement therapy preparations of varying strengths, combinations and routes of administration.
  • NON- HORMONAL ALTERNATIVES
  • -> Phyoestrogens (isoflavones and lignans)
  • -> herbal remedies as Black cohosh, evening primrose oil, St John’s wort
  • COMPLEMENTARY INTERVENTIONS
  • -> acupressure
  • -> hypnotherapy
  • -> reflexology
529
Q

What do systemic HRT preparations target in menopause?

A
  • Hot flushes

- Osteoporosis

530
Q

What do topical HRT preparations target in menopause?

A
  • vaginal dryness
531
Q

What is the definition of HRT?

A

Use of exogenous oestrogens when endogenous secretion is absent

532
Q

What are the main types of HRT preparation?

A
  1. OESTROGEN ONLY
  2. CONTINUOUS COMBINED HRT
  3. SEQUENTIAL COMBINED CYCLICAL HRT
  4. SEQUENTIAL LONG CYCLICAL HRT
  5. TIBOLONE
533
Q

When would Oestrogen only HRT be given?

A

Those with absent uterus

534
Q

When is continuous combined HRT given and how does it work?

A
  • It is a combination of oestrogen and progesterone continuously.
  • Only give if age >54, or if there has been at least >1 year amenorrhoea
  • It is a NO BLEED HRT
535
Q

How does sequential combined cyclical HRT work?

A
  • Oestrogen is taken daily
  • Progesterone is taken for the last 10-14 days of the cycle
  • There will be a withdrawal bleed every month
536
Q

How does sequential long cyclical HRT work?

A
  • Oestrogen is taken for 3 months
  • progesterone is added for the second half of the third month
  • There are withdrawal bleeds every 3 months
537
Q

How does tibolone work?

A
  • Synthetic steroids with estrogenic, androgenic and progestational activity are given
  • there is no withdrawal bleed
538
Q

What are the routes of HRT?

A
  1. oral
  2. patch
  3. gel
  4. implant
  5. topical (vaginal cream, tablet or ring)
539
Q

What are the sources of oestrogen used for HRT?

A
  • SYNTHETIC (from yam and soy beans)

- CONJUGATED EQUINE OESTROGENS

540
Q

What are the sources of progesterone used in HRT?

A

almost all synthetic (derived from plant sources)

  • 17-hydroxyprogesterone
  • 19-nortestorterone derivatives (norethisterone, levonorgestrel)
541
Q

What are the oestrogen related side effects of systemic HRT?

A
  • fluid retention
  • bloating
  • breast tenderness/ enlargement
  • nausea
  • headaches
  • leg cramps
  • dyspepsia
542
Q

What are the progesterone related side effects of systemic HRT?

A
  • fluid retention
  • breast tenderness
  • headaches/migraines
  • mood swings
  • depression
  • acne
  • lower abdominal pain
  • backache
543
Q

What are the side effects of combined systemic HRT?

A
  • irregular, breakthrough bleeding
544
Q

What is a potential side effect of all HRT?

A

WEIGHT GAIN

545
Q

What are the long term benefits of HRT?

A
  1. DECREASE IN VASOMOTOR SYMPTOMS
    (improvement within 4 weeks, maximum therapeutic dose usually achieved by 3 months. Should be continued for at least 1 year)
  2. DECREASE IN UROGENITAL SYMPTOMS AND IMPROVED SEXUALITY
    (improvement may take several months. Long term treatment is often needed as symptoms often recur. Sexuality can be improved with oestrogen alone, but may also need the addition of testosterone)
  3. DECREASED RISK OF OSTEOPOROSIS
    (decreases the risk of spin and hip and other osteoporotic fractures)
  4. DECREASED RISK OF COLORECTAL CANCER
    (by about 1/3)
546
Q

What are the long term risks of HRT?

A
  1. INCREASED RISK OF BREAST CANCER
    (risk dependent on duration of HRT. 5 years after stopping, risk is the same as gen pop.
    Greatest risk with oestrogen-progesterone HRT)
  2. INCREASED RISK OF ENDOMETRIAL CANCER WITH UNOPPOSED OESTROGEN
    (risk increases with prolonged use, risk remains high for 5 or more years after stopping)
  3. INCREASED RISK OF VTE
    (VTE more likely in first year of HRT)
  4. INCREASED RISK OF GALLBLADDER DISEASE
547
Q

What is postmenopausal bleeding?

A
  • Postmenopausal bleeding (PMB) is vaginal bleeding occurring after twelve months of amenorrhoea, in a woman of the age where the menopause can be expected.
548
Q

Causes of postmenopausal bleeding?

A
  • Endometrial carcinoma
  • Endometrial hyperplasia +/- atypia and polyps
  • Cervical carcinoma
  • Atrophic vaginitis
  • Cervicitis
  • Ovarian carcinoma
  • Cervical polyps
549
Q

What is important to consider in postmenopausal bleeding?

A

MUST EXCLUDE CARCINOMA of the endometrium or cervix and premalignant endometrial hyperplasia with cytological atypia.
Withdrawal bleeds occur with sequential HRT, if regular, do not warrant investigation.

550
Q

What investigations are carried out in post menstrual bleeding?

A
  • Bimanual and speculum + smear
  • a TV USS examination with measurement of endometrial thickness can discriminate between women at high and low risk
  • Endometrial biopsy- if malignancy is suspected
  • Hysteroscopy
551
Q

What are the gynecological causes of acute pelvic pain?

A
  • Ectopic pregnancy
  • Ovarian cyst accident (gradual onset, exclusively unilateral dyspareunia and palpation pain)
  • Primary dysmenorrhoea- painful periods
  • Mittleschmerz- ovulation pain, stretchy pain, at time of ovulation
552
Q

What are the non-gynaecological causes of acute pelvic pain?

A

GASTROINTESTINAL

  • appendicitis- nausea/vomiting, no relation to menses (salpingitis more common post menses)
  • IBS/ IBD
  • strangulated hernia

UROLOGICAL

  • UTI
  • Calculi
553
Q

What are the gynecological causes of chronic pelvic pain?

A
  • Pelvic adhesions
  • Fibroids
  • Cervical steroids
  • Asherman’s syndrome
  • dysmenorrhoea
554
Q

What are the non-gynaecological causes of chronic pelvic pain?

A

GASTROINTESTINAL

  • constipation- colicky pain, exacerbated by stress, L-sided/posterior fornix
  • hernias
  • IBS/IBD

UROLOGICAL

  • Interstitial cystitis
  • recurrent small calculi
555
Q

What is endometriosis?

A

The presence of endometrial tissue outside the uterine cavity

556
Q

What are the common sites of endometriosis?

A
  • Peritoneum
  • Pouch of Douglas
  • Ovary/ Fallopian tube
  • Ligaments
  • Bladder
  • Myometrium (adenomyosis)
557
Q

What are the uncommon sites of endometriosis?

A
  • lungs
  • brain
  • muscle
  • eye
558
Q

What are the differentials for endometriosis?

A
  • PID
  • ADHESIONS
  • OVARIAN CYST
  • IBS
559
Q

What are the symptoms associated with endometriosis?

A
  1. Dysmenorrhoea
  2. Cyclical or constant pelvic pain
  3. Dyspareunia (deep indicates possible involvement of uterosacral ligaments)
  4. Urinary symptoms: dysuria (involvement of bladder peritoneum or invasion into bladder)
  5. Rectal/anal symptoms: dyschezia (constipation), cyclic parental bleeding
  6. Chronic fatigue
  7. Caesarean section/ termination of pregnancy
  8. Infertility
560
Q

What are the investigations for endometriosis?

A
  • USS: endometriomas are present- “chocolate cysts”

- Diagnostic laparoscopy: with biopsy for histological verification

561
Q

What are the indications for laparoscopy investigation in endometriosis?

A
  • NSAID resistant lower abdominal pain/dysmenorrhoea
  • pain resulting in days off work/school or hospitalization
  • pain and infertility investigation
562
Q

What is the medication management of endometriosis?

A
  • Analgesia- NSAIDs (symptom relief)
  • Combined oral contraceptives (ovarian suppression)
  • Progestogens
  • Gonadotrophin releasing hormone (GnRH) analogues +/- hormone replacement therapy
  • intrauterine system (IUS) (endometrial and ovarian suppression)
563
Q

What is the surgical management of endometriosis?

A
  • Laparoscopic laser ablation of endometriosis spots
  • Laparoscopic resection of active lesions/scar tissue
  • Laparoscopic cystectomy/oophprectomy
  • Hysterectomy
564
Q

What is PID?

A

Pelvic Inflammatory Disease is the inflammation of a woman’s reproductive organs: the womb, fallopian tubes, ovaries and surrounding tissues. In around 25% of cases, PID is caused by an STI

565
Q

What are the causes of PID?

A
  • Neisseria gonorrhoea
  • Chlamydia trachomatis
  • Bacterial vaginosis associated organisms
  • Other organisms (streptococci, staphylococci, E.coli)
  • Mycoplasma genitalium
  • Mycobacterium tuberculosis
566
Q

What are the risk factors of PID?

A
  1. Age <25
  2. Previous STI
  3. New/multiple sexual partners
  4. Uterine instrumentation such as surgical TOP and IUDs
  5. Postpartum endometritis
567
Q

What are the main symptoms suggestive of PID?

A
  • Lower abdominal pain
  • Cervical excitation
  • Adnexal tenderness
  • Temperature >38
  • Vaginal discharge
  • Dyspareunia
568
Q

What are the main components to discuss in a history of potential PID?

A
  • BLEEDING
  • -> LMP? PCB? IMB? recent onset of menorrhagia?
  • SEXUAL HISTORY
  • -> recent change in partner? vaginal discharge?
  • PAIN
  • -> timing of the pain in relation to menses? dysuria? dyspareunia (deep, sudden onset, constant) bowel pain?
  • OTHER
  • -> fever? (associated with UTI, appendicitis and more severe PID)
569
Q

What are the main investigations for PID?

A
  1. Pregnancy test
  2. Urine dipstick + MSU
  3. Vulvovaginal swabs (chlamydia, gonorrhoea)
  4. HVS for bacterial vaginosis, trichomonas, candida
  5. Temperature
  6. Bloods for HIV/syphilis
  7. Bloods for FBC, ESR/CRP, LFTs
  8. USS if abscess is suspected
570
Q

What is the clinical criteria for diagnosing PID?

A

LOWER ABDOMINAL PAIN plus one:

  • pyrexia
  • leucocytosis
  • ESR > 15

OR one:

  • adnexal pain
  • cervical motion tenderness
  • adnexal mass
571
Q

What are the potential complications of PID?

A
  • Ectopic pregnancy
  • Tubal factor infertility
  • Chronic dyspareunia and pelvic pain
  • Fitz- Hugh Curtis syndrome
572
Q

What are the management options for PID?

A

QUAD A

  • Analgesia
  • Abstinence from sex until both patient and partner have completed treatment and follow up
  • Antibiotic regime
  • Admission for IV therapy in more severe disease (surgical cause has not been excluded, severe symptoms, failure to respond to outpatient management, tube-ovarian abscess suspected)
573
Q

What is the antibiotic regime for managing PID?

A

Ceftriaxone 500mg IM followed by Doxycycline 100mg BD PO 14 days and Metronidazole 400mg BD PO 7-14 days

OR

Ofloxacin 400mg BD PO 14 days and metronidazole 400mg BD PO 14 days

574
Q

What is ‘functional pain’?

A

Intermittent or constant pain in the lower abdomen or pelvis of at least 6 months’ duration, not occurring exclusively with menstruation or intercourse and not associated with pregnancy.
PSYCHOSOMATIC AETIOLOGY

575
Q

What is the investigation and management for ‘functional pain’?

A
  • Transvaginal scan, trial of OCP/ GnRH analogues for 3-6 months (Mirena)
  • Antispasmodics, analgesia, refer to pain clinic
  • Laparoscopy in certain cases
576
Q

What is miscarriage?

A

The loss of a pregnancy before viability. It includes all pregnancy losses before 24 weeks. Majority of miscarriages occur before 12 weeks.

577
Q

What are some of the causes of miscarriage?

A
  1. Fetal abnormality
  2. Sporadic chromosomal abnormalities (most common)
  3. Structural malformations such as major neural tube defects
  4. Acute pyrexial illness
  5. Uterine malformations e.g. bicornuate uterus
  6. Chronic maternal disease such as chronic renal failure etc.
  7. Maternal age
578
Q

What are the considerations in a history of miscarriage?

A
  • VAGINAL BLEEDING (amount and type of loss varies with type of miscarriage and gestation)
  • ABDOMINAL PAIN
  • REGRESSION OF PREGNANCY SYMPTOMS
579
Q

What investigations are done to determine miscarriage?

A
  • clinical history and examination
  • blood group and rhesus factor
  • pregnancy test
  • USS- transvaginal
  • serum hCG- increasing if viable, decreasing if complete miscarriage
580
Q

What should be seen on USS for a normal transvaginal scan?

A
  • Gestation sac appears in the uterus, seen on USS at 5 weeks
  • Gestation sac may contain a yolk sac
  • 5mm fetal pole can be seen at 6 weeks gestation
  • Fetus then doubles in size every week until 12 weeks
581
Q

What would a “non-viable” pregnancy present with?

A

Presence of SAC and FETUS but with no heartbeat. The cut off is 7mm (for the fetal pole), if at 7mm there is no heartbeat, the pregnancy is non-viable.

582
Q

What are the five types of miscarriage?

A
  1. THREATENED MISCARRIAGE
  2. INEVITABLE MISCARRIAGE
  3. COMPLETE MISCARRIAGE
  4. INCOMPLETE MISCARRIAGE
  5. MISSED OR DELAYED MISCARRIAGE
583
Q

What is a threatened miscarriage?

A
  • Where there are symptoms of bleeding +/- pain to suggest miscarriage, but the pregnancy continues.
  • On examination, the cervical os is closed and the uterine size is correct for dates.
  • No harm done and no management required
584
Q

What is an inevitable miscarriage?

A
  • Presents in the process of miscarriage and nothing can be done to save the pregnancy. There is vaginal bleeding and the cervical os is open.
585
Q

What is a complete miscarriage?

A
  • The process is completed without intervention.
  • Patient presents with bleeding which has now lessened
  • Completely empty uterus with thin endometrium
586
Q

What is an incomplete miscarriage?

A
  • Not all of the products of conception have been expelled from the uterus by the miscarriage process.
  • There is continued bleeding, the cervical os remains open and a scan shows debris in the uterus
  • Medical/ surgical management may be required to complete the miscarriage
587
Q

What is a missed/delayed miscarriage?

A
  • The entire gestational sac, which may include the embryo, is retained within the uterus.
  • The pregnancy has stopped growing or developing and the fetal heart has stopped.
  • The cervical os is closed, but the uterus is smaller than the gestational age.
588
Q

What is the expectant management for miscarriage?

A
  • Allow the body to complete the miscarriage “naturally”
589
Q

What is the medical management for miscarriage?

A
  • Prostaglandin and progesterone receptor blocker (misoprostol and mifepristone M&M) to induce uterine contractions to expel remaining products of conception.
  • Can take place in hospital or at home
  • Takes 1-14 days to work
  • Can be complicated by heavy bleeding and moderate abdominal pain
590
Q

What is the surgical management for miscarriage?

A
  • Most common procedure
  • Minor surgical procedure called “evacuation of the uterus” usually under general anesthetic
  • Can do a manual vacuum aspiration done under local anesthetic
591
Q

What is an ectopic pregnancy?

A
  • Implantation of the fertilized ovum outside the body of the uterus. Over 90% are tubal ectopic, with the rest being abdominal, ovarian, cervical or rarely in CS scars.
592
Q

What are the risk factors for ectopic pregnancy?

A
  1. PID esp. chlamydia
  2. Previous ectopic pregnancy
  3. Pelvic, tubal surgery
  4. Sterilisation/ reversal of sterilization
  5. Use of IUD
  6. Endometriosis
  7. Assisted contraception, especially IVF
  8. Smoking
593
Q

What are the symptoms associated with ectopic pregnancy?

A
  • unilateral, lower abdominal abdominal pain
  • Vaginal bleeding/ irregular vaginal bleeding over 2-3 weeks (often small amount and brown)
  • diarrhea and vomiting
  • Severe shoulder tip pain- diaphragmatic irritation from intra-abdominal blood
  • Collapse- if ruptured
594
Q

What are the signs associated with ectopic pregnancy?

A
  • Abdominal tenderness
  • cervical excitation due to stretching of inflamed tissues
  • unilateral adnexal tenderness
  • adnexal mass
  • peritonism due to intra-abdominal blood
595
Q

What investigations are done in ectopic pregnancy?

A
  1. PREGNANCY TEST- negative test confidently excludes an ectopic
  2. SERUM hCG- Take 48hrs apart- (a rise of >66% suggests an intrauterine pregnancy. Suboptimal rise is suspicious of an ectopic)
  3. SERUM PROGESTERONE- is helpful to distinguish whether a pregnancy is failing.
  4. TRANSVAGINAL USS- confirm an intrauterine pregnancy (won’t identify ectopic)
  5. LAPAROSCOPY- definitive diagnosis and is advised if doubt exists
596
Q

What is the medical management for an ectopic pregnancy?

A

METHOTREXATE IM 50mg/m2

  • This takes 4-6 weeks to resolve.
  • serum hCG levels should be measured at 4 days and 7 days

recommended for cervical and corneal ectopics in particular

597
Q

Considerations for management of ectopic pregnancy

A
  • Women managed expectantly and medically should be counseled about the importance of compliance with follow up and should be within easy access of the hospital.
598
Q

What is a molar pregnancy/ trophoblastic disease?

A

Trophoblastic tissue (the part of the blastocyst that normally invaded the endometrium) proliferates aggressively. Proliferation can be local and non-invasive (hydatidiform mole)

599
Q

What is a complete hydatidiform mole?

A
  • Sperm fertilises an ‘empty’ egg (no chromosomes/genetic material)
  • This ovum implants and trophoblast cells grow and develop as disorganized tissue- but embryo doesn’t develop.
  • There is no fetal tissue at all
600
Q

What is a partial hydatidiform mole?

A
  • Conception does not take place normally
  • Two sperm fertilizing one egg- too much genetic material
  • Growth of trophoblastic tissue overtakes the growth of any fetal tissue and the fetus does not develop normally.
601
Q

What is the presentation of a hydatidiform mole?

A
  • PREGNANCY SYMPTOMS- (amenorrhoea, nausea, vomiting, breast tenderness)
  • BLEEDING (most common symptom- many women think it is a miscarriage)
  • NO SYMPTOMS- can be incidental finding on USS
  • RARE SYMPTOMS- HTN, HG
602
Q

What investigations are done for hydatidiform mole?

A
  • USS
  • serum hCG
  • CXR (cannonball/snowstorm appearance)
  • CT chest/ abdomen
603
Q

What are the management options for hydatidiform mole?

A
  1. REMOVE THE MOLE- suction curettage in theatres
  2. CHEMO if malignant
    - -> low risk patients receive methotrexate with folic acid
    - -> high risk receive risk combination chemotherapy
604
Q

How is the chemotherapy regime for molar pregnancy determine?

A
  • Age of the patient and type of antecedent pregnancy
  • Extent of tumor burden (hCG level, number, size of tumor, size of mets)
  • Interval from antecedent pregnancy
  • Response to previous chemotherapy
605
Q

How does malignancy present when followed from molar pregnancy?

A
  • persistently elevated or rising hCG levels
  • persistent vaginal bleeding
  • evidence of blood-borne metastasis, commonly to the lungs
606
Q

What are fibroids (leiomyomata)?

A

Benign tumors arising from the myometrium of the uterus.

607
Q

What are the symptoms for fibroids?

A
  • They are usually asymptomatic
  • dysmenorrhoea, menorrhagia, pressure symptoms (frequency), pelvic pain and infertility
  • IN PREGNANCY- pain, abnormal lie, obstruction if cervical, difficulty in CS
608
Q

How do fibroids grow?

A

Growth is oestrogen and progesterone dependent.

Fibroids regress after the menopause due to reduction in circulating oestrogen.

609
Q

What are the types of uterine fibroids?

A
  • SUBMUCOUS
  • -> >50% projection into the endometrial cavity
  • INTRAMURAL
  • -> located within the myometrium
  • SUBSEROUS
  • -> >50% of the fibroid extends outside the uterine contours
  • CERVICAL
  • PEDUNCULATED
  • -> mobile and prone to torsion
  • PARASITIC
  • ->have become detached from the uterus and attached to other structures.
610
Q

What are the investigations for fibroids?

A
  • Clinical examination (hard, irregular, uterine mass)

- Transvaginal or abdominal ultrasound can differentiate types and dimensions.

611
Q

What is the management for fibroids?

A
  • GnRH to shrink fibroids prior to surgery
  • Myomectomy- open laparoscopic, hysteroscopic.
  • Hysterectomy (women >45, or who have finished their family- guaranteed cure of fibroids)
  • Uterine artery embolization (uterine artery is catheterized)
612
Q

What are the complications for fibroids?

A
  • Torsion of pedunculate fibroid
  • calcification
  • leiomyosarcoma
613
Q

How can you tell if a fibroid is malignant?

A
  • pain and rapid growth
  • growth in postmenopausal women not in HRT
  • poor response to GnRH agonist
614
Q

What are ovarian cysts?

A

Common and physiological cysts.

- FOLLICULAR CYST (<3cm) and CORPUS LUTEAL CYST (<5cm) during the menstrual cycle

615
Q

What are some common PREMENOPAUSAL ovarian masses?

A
  • follicular/luteal cysts
  • dermoid cysts
  • endometriomas
  • benign epithelial tumour
616
Q

What are some common POSTMENOPAUSAL ovarian masses?

A
  • Benign epithelial tumour

- Malignancy

617
Q

What are the symptoms/ presentation for ovarian cysts?

A
  • ASYMPTOMATIC
  • Chronic pain: dull ache, pressure on other organs, dyspareunia, cyclical pain
  • Acute pain: bleeding, torsion, rupture
  • Abnormal uterine bleeding
  • Hormonal effects
618
Q

What should be asked in a history of ovarian cysts?

A
  • Menstrual history (LMP, cycle length, menorrhagia)
  • Pain (site, nature, radiation (usually down leg), duration, precipitating factors)
  • bowel/bladder function
  • abdominal distension
  • medical/ family history
619
Q

What is done in an examination for the investigation of ovarian cysts?

A

SYSTEMIC: pulse, BP, anaemia, temperature
ABDOMINAL: mass arising from the pelvis, tenderness, peritonism, upper abdominal aches
PELVIC: PV discharge/ bleeding; cervical excitation; adnexal mass or tenderness

620
Q

Which haematologcial tests are done when investigating ovarian cysts?

A
  • FBC
  • tumour markers
  • CA125
  • AFP, hCG, LDH, inhibin, oestradiol
621
Q

What imaging is done when investigating ovarian cysts?

A
  • ABDOMINCAL/ PELVIC USS (may indicate presence and appearance of pelvic mass and ascites)
622
Q

What is the general management for ovarian cysts?

A
  • ANALGESIA, as most resolve spontaneously

- Urgent LAPAROSCOPY if there are signs of torsion/rupture/ hemorrhage.

623
Q

What is the management for adolescent women with ovarian cysts?

A
  • Germ cell tumors are more common in this age group therefore aim for conservative surgery (cystectomy) to diagnose, but preserve fertility.
624
Q

What is the management for premenopausal women with ovarian cysts?

A
  • Exclude malignancy and preserve fertility
  • re-scan in 6 weeks
  • monitor cyst with USS and CA125. Calculate RMI
625
Q

What is the management for postmenopausal women with ovarian cysts?

A

Low RMI (<25) follow up for 1 year with USS and CA125 every 4 months. If change and RMI still low or woman requests removal, LAPAROSCOPIC OOPHORECTOMY

Moderate RMI (25-250) OOPHORECTOMY in cancer centre is recommended. If malignancy found, then full staging laparotomy needed.

High RMI (>250) Refer to cancer centre for a full staging laparotomy

626
Q

What is the management for low risk cysts?

A
  • Transvaginal cyst aspiration under USS guidance
  • If persistent cyst, consider laparoscopic cystectomy
  • If cyst <5cm and simple, cyst fenestration and wall biopsy
  • if cyst >5cm or is dermoid, prevent spillage of contents and remove cyst in a “endobag”
627
Q

How to tell if an ovarian cyst is malignant?

A
  • rapid growth >5cm
  • ascites
  • advanced age
  • bilateral masses
  • solid or septante nature on ultrasound scan
  • increased vascularity
628
Q

What is the definition of incontinence?

A

Objectively demonstrable involuntary loss of urine which is a social or hygienic problem. 40% of women suffer from some form of incontinence in their lives

629
Q

What are the main types of incontinence?

A
  1. STRESS
  2. URGE
  3. MIXED
  4. OVERFLOW
  5. CONTINUOUS
630
Q

What is stress incontinence?

A
  • Involuntary leakage of urine on effort or exertion, or on sneezing or coughing.
  • It commonly arises as a result of URETHRAL SPHINCTER WEAKNESS
631
Q

What is urge incontinence?

A
  • Involuntary leakage of urine accompanied by, or immediately preceded by, a strong desire to pass urine (void).
  • Urge urinary incontinence can be a symptom of OVERACTIVE BLADDER SYNDROME
632
Q

What is mixed incontinence?

A
  • Involuntary leakage of urine associated with BOTH urgency and with exertion, effort, sneezing or coughing.
  • Usually one of these is predominant, i.e. the symptoms of either stress/urger incontinence is more bothersome.
633
Q

What is overflow incontinence?

A
  • Occurs when the bladder becomes large and flaccid and has little or no DETRUSOR TONE/FUNCTION.
  • This is usually due to injury or insult e.g. after surgery/postpartum.
  • The condition is diagnosed when the urinary residual is >50% of bladder capacity.
  • The bladder simply leaks when it becomes full.
634
Q

What is continuous incontinence?

A
  • The complaint of continuous leakage

- Classically associated with a fistula or congenital abnormality e.g. ectopic ureter

635
Q

What are the 12 main symptoms of incontinence?

A
  1. DAYTIME FREQUENCY
  2. NOCTURIA
  3. NOCTURNAL ENURESIS (incontinence during sleep)
  4. URGENCY
  5. VOIDING DIFFICULITIES
  6. POSTMICTURITION
  7. ABSENT OR REDUCED BLADDER SENSATION
  8. BLADDER PAIN (indicative of intravesical pathology)
  9. URETHRAL PAIN
  10. DYSURIA
  11. HAEMATURIA
  12. PROLAPSE SYMPTOMS
636
Q

What is associated with voiding difficulties in incontinence?

A
  • hesitancy (difficulty initiating micturition)
  • straining to void
  • slow or intermittent urinary stream
637
Q

What is associated with postmicturition in incontinence?

A
  • feeling of incomplete bladder emptying
  • terminal dribble (a prolonged final part of micturition)
  • postmicturitional dribble (involuntary loss of urine immediately after passing urine).
638
Q

What main points should be covered in a history of incontinence?

A
  • Urological history (incontinence, frequency, voiding, UTIs)
  • Gynae history (menstrual, prolapse, surgery)
  • Obstetric history (parity, MOD, birth weights)
  • Medical history (resp, cardiac, GI, CNS, DM, psych)
  • Drug history (diuretics, beta blockers, anticholinergics)
  • Incontinence (onset, stress/urge, volume, frequency)
  • Irritative (affects of incontinence- frequency, urgency, nocturne, dysuria)
  • Voiding (poor stream, straining, prolonged, incomplete emptying)
  • Other (UTI, nocturnal enuresis, childhood problems, retention, catheterisation)
  • QoL
639
Q

What should be assessed during an examination of a patient with incontinence?

A
  • BMI
  • Abdominal exam (check for pelvic masses)
  • Post-menopausal atrophy- check condition of the vulval skin
  • Vaginal discharge
  • Prolapse
  • Incontinence
640
Q

What investigations should be done in a patient with incontinence?

A
  • Thorough history and examination
  • Urine dipstick/ MSU
  • Frequency/ volume charts (quantification of fluid intake and voiding behavior)
  • Urodynamics (assessment of bladder function in and out patient setting. The bladder is filled and emptied whilst pressure readings are taken)
641
Q

What is urodynamic stress urinary incontinence (USI)?

A

Involuntary leakage of urine during increased intra-abdominal pressure in the absence of detrusor contractions. It can only be diagnosed by urodynamic testing.

642
Q

What are common risk factors of stress urinary incontinence?

A
  • age
  • menopause
  • vaginal delivery
  • prolapse
  • previous bladder neck surgery
643
Q

What will a frequency/volume chart show in stress urinary incontinence?

A
  • normal frequency
  • functional bladder capacity
  • slightly increased diurnal frequency
644
Q

What is the conservative management for stress urinary incontinence?

A
  1. LIFESTYLE INTERVENTION (weight reduction, smoking cessation, treatment of constipation/chronic cough)
  2. PELVIC FLOOR MUSCLE TRAINING (for at least 3 months)
  3. ELECTRICAL STIMULATION
  4. VAGINAL CONES
645
Q

What is the pharmacological management for stress urinary incontinence?

A

DULOXETINE- only drug licensed for moderate to severe stress urinary incontinence

  • it is an SNRI
  • it enhances urethral striated sphincter activity via a centrally mediated pathway
  • nausea is the most common side effect
646
Q

What is the surgical management for stress urinary incontinence?

A
  • PERIURETHRAL INJECTIONS
  • COLPOSUSPENSION
  • TAPES (tension free vaginal tape or transobturator tape)
647
Q

What is TVT?

A
  • tension free vaginal tape

- a polypropene tape is placed under mid urethra via a small vaginal incision.

648
Q

What is overactive bladder syndrome (OAB)?

A
  • Chronic condition
  • defined as urgency (with or without urge incontinence)
  • implies underlying detrusor overactivity
  • most common cause of incontinence in elderly women
649
Q

What are the symptoms associated with urge incontinence?

A
  • urgency (strong desire to void)
  • urge incontinence
  • nocturnal enuresis
  • triggered by provocative factors (e.g. hearing running water, cold weather etc)
650
Q

What can be seen on a frequency/volume chart in urge incontinence?

A
  • increased diurnal frequency associated with urgency

- nocturia

651
Q

What can be seen in urodynamic investigations of urge incontinence?

A
  • if involuntary bladder muscle activity causes an increase of pressure in the bladder and leads to leaking.
652
Q

What is the conservative management for urge incontinence?

A
  • reduce tea/ coffee
  • smoking cessation
  • bladder retraining
653
Q

What is the pharmacological management for urge incontinence?

A
  • Anticholinergics

- Desmopressin

654
Q

What is the surgical management for urge incontinence?

A
  • Intravesical botox
  • sacral nerve stimulation
  • neuormodulator implant
  • cystectomy
655
Q

What is prolapse?

A

Protrusion of the UTERUS and or VAGINA beyond normal anatomical confines.
Bladder, urethra, rectum and bowel are also often involved

656
Q

What are the main causes for prolapse?

A
  • PREGNANCY and VAGINAL DELIVERY
  • CONGENITAL FACTORS
  • MENOPAUSE
  • CHRONIC PREDISPOSING FACTORS (chronic increase in intraabdominal pressure e.g. obesity, chronic cough, constipation, heavy lifting or pelvic mass)
  • IATROGENIC FACTORS
657
Q

What is prolapse of the anterior compartment?

A
  • urethrocele

- cystocele (bladder)

658
Q

What is prolapse of the mid compartment?

A
  • Uterine

- Vaginal vault

659
Q

What is prolapse of the posterior compartment?

A
  • rectocele

- enterocoele (bowel)

660
Q

What is the commonly used grading system for pelvic organ prolapse?

A
  1. No descent of pelvic organs during straining
  2. Leading surface of prolapse does not descend below 1cm above the hymenal ring
  3. Leading edge of the prolapse extends from 1cm above to 1cm below the hymenal ring
  4. Prolapse extends 1cm or more below hymenal ring but without complete vaginal eversion
  5. Vaginal completely everted (complete procidentia)
661
Q

What are the general symptoms associated with prolapse?

A
  • dragging sensation, discomfort, heaviness within the pelvis
  • feeling of a ‘lump coming down’
  • dyspareunia or difficulty in inserting tampons
  • discomfort and backache
662
Q

What are the symptoms associated with cysto-urethrocele in prolapse?

A
  • urinary urgency and frequency
  • incomplete bladder emptying
  • urinary retention or reduced flow where the urethra is kinked by descent of the anterior vaginal wall
663
Q

What are the symptoms associated with rectocele in prolapse?

A
  • constipation

- difficulty with defecation (may digitally reduce it to defecate)

664
Q

How is prolapse investigated?

A
  • Clinical examination

- Sims’ speculum examination of the vaginal walls

665
Q

What is an important consideration for grade 3 or 4 prolapse?

A
  • mucosal ulceration may be present and lichenification, resulting in vaginal bleeding and discharge.
666
Q

What is the conservative management for prolapse?

A
  • Weight reduction (BMI <30)
  • Pelvic floor exercises
  • Treatment of chronic constipation
  • Treatment of chronic cough (including smoking cessation)
667
Q

What is the pharmacological management for prolapse?

A

INTRAVAGINAL DEVICES

  • ring pessary- placed between posterior aspect of the symphysis pubis and posterior fornix
  • shelf pessary
668
Q

What is the surgical management for prolapse?

A
  • anterior repair (bladder)
  • posterior repair
  • vaginal hysterectomy
  • use of vaginal mesh
669
Q

What is painful bladder syndrome/ interstitial cystitis?

A
  • inflammatory disorder causing pain, urinary symptoms and dyspareunia
  • chronic inflammation of the bladder wall
670
Q

What are the symptoms associated with painful bladder syndrome?

A
  • pain with bladder filling
  • suprapubic pain
  • frequency, urgency, nocturia
  • cyclical exacerbation can occur and pain is often relived by voiding
671
Q

What are the causes of painful bladder syndrome?

A
  • may coexist with other pathologies

- no bacterial infection/ recurrent UTIs with negative cultures

672
Q

How is painful bladder syndrome diagnosed?

A
  • Cystoscopy

- Biopsy

673
Q

What is the conservative management for painful bladder syndrome?

A
  • diet and fluid advice
  • support groups
  • referral to pain team
674
Q

What is the pharmacological management for painful bladder syndrome?

A
  • amitriptyline, nortriptyline, cimetidine
  • antimuscarinics- trospium, solifenacin
  • 6 months low dose antibiotics
  • Elmiron
675
Q

What are the risk factors for endometrial cancer?

A

PRESENCE OF UNOPPOSED OESTROGEN

  1. OBESITY- oestrogen from aromatization of adrenal androgens in fat tissue
  2. DIABETES- 4x higher especially if obese
  3. REDUCED ENDOGENOUS PROGESTERONE PRODUCTION (PCOS, early menarche, late menopause, nulliparity)
  4. AGE
  5. FAMILY HISTORY (breast, ovarian, colon cancer)
  6. TAMOXIFEN USE
  7. PELVIC IRRADIATION
676
Q

What are the different types of endometrial tumor?

A
  • ENDOMETROID ADENOCARCINOMA (80-85%)
  • PAPILLARY SEROUS (10%)
  • CLEAR CELL (4%)
677
Q

What are the protective factors for endometrial cancer?

A
  • pregnancy
  • diet
  • exercise
  • IUS
  • reduced menstrual history
  • COCP
678
Q

What are the modes of spread of endometrial cancer?

A
  • DIRECT- through cavity to cervix, fallopian tubes to ovaries/peritoneum.
  • LYMPHATIC- pelvic> para-aortic nodes
  • HAEMATOGENOUS- rare to liver, lunges
679
Q

How does endometrial cancer present?

A
  • POST MENOPAUSAL BLEEDING
  • menstrual disturbance in younger patients
    PV discharge/ pyometra may occur instead of bleeding. Have increased suspicion in postmenopausal women with increased PV discharge
680
Q

What are the investigations for endometrial cancer?

A
  • Examination- speculum, pelvic exam
  • Biopsy +/- hysteroscopy
  • USS- endometrial thickness and suspicious appearances
  • MRI invasion
  • CT abdo/chest if high risk cancer
681
Q

How is endometrial cancer staged?

A
  1. UTERUS ONLY
    » 1a. < 1/2 myometrial invasion
    » 1b. > 1/2 myocetrial invasion
  2. CERVIX ALSO
  3. PELVIC/ PARA-AORTIC LYMPH NODES
  4. BOWEL AND BLADDER OR DISTANT SPREAD
682
Q

What is the pharmacological management for endometrial cancer?

A

Hormonal therapy (progesterone) can reverse the premalignant phase of hyperplasia- this is usually palliative

  • high dose progesterone used for advanced and recurrent disease
  • aiming for palliation of symptoms
683
Q

What is the surgical management for endometrial cancer?

A
  • total abdominal hysterectomy and bilateral sapling-oophercetomy and pelvic washings.
  • In obese women, laparoscopy is best +/- pelvic lymphadenectomy
684
Q

What is the radiotherapy management for endometrial cancer?

A

Adjuvant chemotherapy is reserved for women with high grade, high stage tumours

685
Q

What is the premalignant stage of endometrial cancer?

A

Hyperplasia with atypia- excessive proliferation of endometrial glands and stroma

  • simple= 3% risk of progression to cancer
  • complex= 3% risk of progression to cancer
  • complex with atypia= 25-30% risk of progression to cancer over 10 years
686
Q

What are the risk factors for cervical cancer?

A
  1. EXPOSURE TO HPV
    - -> early 1st sexual experience
    - -> multiple partners
    - -> non-barrier contraceptive
    - -> Previous STI
  2. COCP and high parity
  3. SMOKING (reduces viral clearance)
  4. IMMUNOSUPPRESSION: HIV and transplant patients especially
687
Q

What is one of the biggest causes/ associations of cervical cancer?

A

Persistent infection with high risk human papilloma virus

HPV subtypes 16 and 18

HPV causes the production of 2 proteins known as E6 and E7 which turn off some tumor suppressor genes.

688
Q

What is the presentation of cervical cancer?

A
  • Post-coital bleeding
  • persistent, offensive, blood-stained discharge
  • post menopausal bleeding
  • cervical smear demonstrating potential invasion
  • incidental at treatment for pre-invasive disease (CIN)
689
Q

What are the presentations of cervical cancer that suggest advanced disease?

A
  • heavy bleeding PV
  • ureteric obstruction- renal failure
  • weight loss
  • bowel disturbance
  • fistula (vesicovaginal)
  • swollen leg from a pelvic thrombosis
690
Q

What investigations are given for cervical cancer?

A

EXAMINATION

  • Vaginal and bimanual examination: will show
  • -> roughened, hard cervix
  • -> potential loss of fornices
  • -> fixed cervix

HISTOLOGY
- Punch biopsy or small loop biopsy at colposcopy

  • U&Es, LFTs, FBC
  • CXR for staging and pre-op assessment
  • MRI
691
Q

What are the stages for cervical cancer?

A
  1. CARCINOMA IN SITU
  2. CONFINED TO CERVIX
  3. DISEASE BEYOND CERVIX- but not to pelvic wall or lower 1/3 of the vagina
  4. DISEASE TO PELVIC WALL/ LOWER 1/3 OF THE VAGINA
  5. INVADES BLADDER, RECTUM, OR METASTASIS
692
Q

What are the modes of spread of cervical cancer?

A
  • DIRECT or LOCAL- vagina, bladder, parametric bowel
  • LYMPHATIC- parametrical nodes, internal, external and common iliac nodes, obturator nodes, pre-sacral and para-aortic nodes
  • HAEMATOGENOUS- liver, lungs
693
Q

What are the general management options for cervical cancer?

A
  • LLETZ (large loop excision of the transitional zone)
  • hysterectomy
  • radical hysterectomy
  • fertility sparing trachelectomy
  • radiotherapy
  • chemotherapy
694
Q

What is the premalignant stage of cervical cancer?

A

CIN (cervical intraepithelial neoplasia)- depends on the level from the basement membrane involved.

CIN1- 1/3 thickness involved
CIN2- 2/3 thickness involved
CIN 3- all of the thickness of epithelium involved

695
Q

What are the time scales for cervical screening?

A
  • 25- 49- screened every 3 years

- 50- 64- screened every 5 years

696
Q

What is the management for cervical cancer dependent on stage?

A

1a(i)- cone biopsy or simple hysterectomy
1a (ii)- 1b (i)- laparoscopic lymphadenectomy and radical trachelectomy to preserve fertility

Stage 1a (ii)- 2a: LNs negative- Wertheim’s hysterectomy or chemo-radiotherapy OR LNs positive- chemo-radiotherapy without surgery

Stage 2b-4: Chemo-radiotherapy without surgery.

697
Q

What are the available HPV vaccinations?

A

GARDASIL- protects against the two types of HPV and prevents against genital warts

HPV types- 6/11/16/18
oncogenes- 16/18/31/33

698
Q

What are the risk factors for ovarian cancer?

A
  • those at increased risk of multiple ovulations
  • nulliparity
  • early menarche/ late menopause
  • HRT use
  • endometriosis
  • difficulties conceiving
  • genetic - BRCA1 and 2
  • Turner’s syndrome
699
Q

What are some factors that decrease the risk of ovarian cancer?

A
  • those with ovulation suppressed
  • use of the COCP
  • pregnancy
700
Q

What are the associated symptoms with ovarian cancer?

A
  • abdominal swelling
  • pressure effects on the bladder and rectum
  • dyspnoea
  • gastrointestinal upset and anorexia
  • detection of mass
  • abnormal vaginal bleeding
  • asymptomatic
701
Q

What can be detected on clinical examination in ovarian cancer?

A
  • adnexal or pelvic mass
  • shifting dullness
  • irregular abdominal mass
  • pleural effusion
  • lymph nodes (supraclavicular)
702
Q

Which tumor markers are investigated in ovarian cancer?

A

TUMOUR MARKERS

  • CA125 expressed by 80% of epithelial ovarian tumors
  • CA19.9- mucinous- testing for metastases from pancreas
  • carcinoembryonic antigen CEA- testing for metastases from bowel
  • AFP, HCG, LDH
703
Q

What are the other investigations of ovarian cancer?

A
  • pelvic ultrasound
  • CXR (effusion or lung mets)
  • FBC, U&Es, LFTs0 especially albumin
  • CT abdomen and pelvis
  • Paracentesis of ascites
704
Q

What is the mode of spread for ovarian cancer?

A
  • DIRECT- mental cake, invasion to bowel, bladder
  • HAEMATOGENOUS- liver and spleen
  • LYMPHATIC SPREAD- para-aortic to diaphragmatic lymph nodes
705
Q

What is the staging for ovarian cancer?

A

STAGE 1- LIMITED TO OVARIES

1a. One ovary
1b. Both ovaries
1c. Ruptured capsule, surface tumor, positive peritoneal washings/ascites

STAGE 2- LIMITED TO PELVIS

2a. uterus, tubes
2b. other pelvic structures
2c. 2a+2b AND positive peritoneal washings/ ascites

STAGE 3- LIMITED TO ABDOMEN

3a. microscopic metastases
3b. macroscopic metastases (<2cm)
3c. macroscopic metastases >2cm, regional lymph nodes

STAGE 4- DISTANT METASTASES OUTSIDE ABDOMINAL CAVITY

706
Q

What are the surgical management options for ovarian cancer?

A
  • Laparotomy
  • hysterectomy
  • bilateral sailing-oophectomy
  • omenectomy
  • lymph node sampling (pelvic and para-aortic)
  • peritoneal biopsies
  • pelvic washings/ ascitic sampling
707
Q

What are the chemotherapy options for those with ovarian cancer?

A

Adjuvant chemotherapy is recommended to all (following surgery), other than those with low risk/ early stage disease

6 cycles of CARBOPLATIN +/- PACLITAXEL every 3 weeks

708
Q

What are the risk factors for vulval cancer?

A
  • AGE (over 70)
  • HPV- 16/18/31/33
  • Smoking
  • Immunodeficiency- HIV, immunosuppressants
  • lichen sclerosis- 4% risk of vulvar cancer
  • melanoma- personal or family history
  • previously identified VIN
709
Q

What are the different types of vulvar cancer?

A
  • squamous cell carcinoma (90%)
  • 1st degree vulval melanomas
  • Basal cell
  • Bartholin’s gland carcinoma
  • sarcoma (rarely)
710
Q

What are the premalignant conditions for vulvar cancer?

A
  • Vulvar intraepithelial neoplasia- abnormal cells only found in the surface layer of vulvar skin.
711
Q

What are the symptoms of vulvar cancer?

A
  • ASYMPTOMATIC!
  • itching
  • pain
  • bleeding (PMB)
  • ulcer
  • lump
712
Q

What can be seen on clinical examination of a patient with vulvar cancer?

A
  • skin often thicker and lighter (or darker) that surrounding skin
  • raised mass- red/ pink/ white
  • ulcerated mass
  • warty mass
  • regional lymph nodes
713
Q

What are the investigations for vulvar cancer?

A
  • FBCs, U&Es, LFTs
  • PR, PV, lingual lymphadenopathy (to assess spread)
  • Biopsy
  • MRI to assess spread
  • CXR
714
Q

What is the staging for vulval cancer?

A

STAGE 1- confined to the vulva

STAGE 2- extension to adjacent perineal structures (1/3 lower urethra, 1/3 lower vagina, anus) with negative nodes

STAGE 3- extension to adjacent perineal structures (1/3 lower urethra, 1/3 lower vagina, anus) with positive nodes

STAGE 4- Invasion of other regional structures (2/3 upper urethra, 2/3 upper vagina) or distant structures

715
Q

What is the treatment for vulval cancer?

A
  • Wide local excision of the suspicious area
  • Vulvectomy
  • Ipsilateral/ bilateral lymphadenectomy
  • -> >1mm invasion should have groin lymphadenectomy
  • -> lateral disease can have ipsilateral LN dissection
  • -> positive LN- bilateral groin LN dissection
  • -> central disease= bilateral groin LN dissection
  • Radiotherapy
  • Chemotherapy
716
Q

When should investigation/ referral be made for subfertility?

A
  • female age >35
  • known fertility problems
  • anovulatory cycles
  • severe endometriosis
  • previous PID
  • malignancy
717
Q

What are some causes of infertility?

A
  • Male factor
  • Anovulatory infertility
  • Tubal disease
  • Endometriosis
  • Unexplained
718
Q

What 9 things should be determined in a history for a couple with subfertility?

A
  1. Age
  2. duration of subfertility and coital frequency
  3. menstrual cycle regularity and LMP
  4. pelvic pain? (dysmenorrhea/ dyspareunia)
  5. cervical smear history
  6. previous pregnancies/ history of ectopic?
  7. previous tubal/ pelvic surgery
  8. previous/ current STIs
  9. previous PID

PMH
DH
FH/SH

719
Q

What should be looked for in clinical examination in subfertility?

A
  • BMI
  • signs of endocrine disorder (hyperandrogenism- acne, hair growth, alopecia), acanthosis nigricans, hypo/hyperthyroidism, visual field defects

pelvic examination

  • obvious pelvic pathology (adnexal mass, uterine fibroids, endometriosis, vaginismus
  • cervical smear
  • chlamydia screening
720
Q

What investigations can be done in primary care for subfertility?

A
  • Chlamydia screening
  • baseline hormone profile (FSH, LG, TSH, PROLACTIN, TESTOSTERONE)
  • rubella status
  • mid-luteal progesterone level
  • semen analysis
721
Q

What are the general recommendations for those with subfertility?

A
  • 0.4mg folic acid
  • smoking cessation/ alcohol cessation (female stop, males reduce)
  • healthy diet
  • regular exercise
  • avoid ovulation induction kits
  • be aware of environmental conditions
722
Q

What can be done to aid ovulation induction?

A
  • weight loss/ gain as appropriate
  • anti-estrogens (clomifene 50mg days 2-6)
  • gonadotrophins or pulsatile GnRH
  • laparoscopic ovarian diathermy
  • insulin sensitizers
  • surgery to treat endometriosis, tubal surgery etc.
723
Q

What is premature (primary) ovarian insuffiency?

A
  • loss of normal function of the ovaries before age 40
  • as the ovary fails, estradiol and inhibin levels are loa, so reduced negative feedback on the pituitary causes FSH and LH levels to rise
724
Q

What can cause tubal damage and lead to subfertility?

A
  • INFECTION (history of PID, infection from TOP/ miscarriage)
  • ENDOMETRIOSIS
  • SURGERY/ ADHESIONS
725
Q

What are the main assisted reproductive technologies used to help fertility?

A
  • IVF (in- vitro fertilisation)
  • ICSI (intra-cytoplasmic sperm injection)
  • PGD (pre-implantation genetic diagnosis)
  • egg donation
  • surrogacy
726
Q

What are the indications for IVF?

A
  • tubal disease
  • male factor subfertility
  • endometriosis
  • anovulation
727
Q

What can effect the success of IVF treatment?

A
  • maternal age
  • duration of subfertility
  • elevated FSH levels may indicate poor response to ovarian stimulation
  • previous failed IVF
728
Q

How does ICSI work?

A
  • single sperm is injected into the ooplasm of the oocyte.

- sperm may be retrieved from ejaculate, or from epididymis or testes.

729
Q

What are some complications associated with assisted conception?

A
  • EGG COLLECTION- Intraperitoneal hemorrhage and pelvic infection
  • PREGNANCY- increased multiple pregnancies, increased rate of ectopic
  • GENETICS
  • MENTAL WELLBEING
  • OVARIAN HYPERSTIMULATION
730
Q

What is ovarian hyperstimulation syndrome (OHSS)?

A
  • ovarian enlargement
  • shifting of fluid from the intravascular to the extravascular space
  • fluid accumulates in the peritoneal and pleural spaces
  • intravascular fluid depletion leading to- haemoconcentration, hypercoaguability
731
Q

What are the risk factors for OHSS?

A
  • polycystic ovaries
  • younger women with low BMI
  • previous OHSS
732
Q

What is are the three objectives for treatment of OHSS?

A
  1. symptomatic relief
  2. prevention of haemoconcentration and thromboembolism
  3. maintenance of cardiorespiratory function
733
Q

What can be done for symptomatic relief in OHSS?

A
  • paracentesis
  • analgesia
  • anti-emetics
734
Q

What can be done for prevention of haemoconcentration and thromboembolism in OHSS?

A
  • assessment of hydration status (FBC, U&Es, LFTs, albumin)
  • assessment of ascites (girth measurement and weight)
  • assessment of legs for thromboembolism
  • compression stockings for thromboprophylaxis
  • consideration of heparin
735
Q

What are the causes for male subfertility?

A
  • IDIOPATHIC
  • VARICOCELE
  • HYPOGONADISMS
  • INFECTION
  • MALDESCENDED TESTES
  • SEXUAL DYSFUNCTION
  • IMMUNOLOGICAL
  • GENERAL AND SYSTEMIC DISEASE
  • OBSTRUCTIONS
736
Q

What investigations should be done in male subfertility?

A
  • FSH
  • karyotype (exclude 47XXY)
  • cystic fibrosis screen (CBAVD)
  • semen analysis
737
Q

What are the WHO recommendations for a normal sperm analysis?

A
VOLUME- >1.5ml
pH- 7.2-8
Count- >15million/ml
Motility- >40%
Progressive motility- >32%
Morphology- >4% normal
Antisperm antibodies- >50%
738
Q

What is oligozoospermia?

A

A sperm count of <15 million/ml

739
Q

What is asthenozoospermia?

A

Reduced sperm motility

740
Q

What is teratozoospermia?

A

Abnormal morphology

741
Q

What are the considerations for sperm analysis?

A
  • Sample should be produced by masturbation with the last ejaculation occurring 2-7 days previously
  • Sample must be analyzed within 1-2h of production
  • Abnormal analysis must be repeated in 12 weeks.
742
Q

What is the management for the male factors of subfertility?

A
  • treat an underlying medical conditions

- address lifestyle issues

743
Q

What medications should be reviewed in treatment of male subfertility?

A
  • antispermatogenic- (alcohol, anabolic steroids, sulfasalazine)
  • antiandrogenic- (cimetidine, spironolactone)
  • erectile/sexual dysfunction (alpha/beta blockers, antidepressants, diuretics, metoclopramide)
744
Q

What are medical treatments available for male subfertility?

A
  • gonadotrophins in hypogonadotrophic hypogonadism

- sympathomimetics (imipramine) in retrograde ejaculation

745
Q

What is the surgical management for male subfertility?

A
  • relieve obstruction
  • vasectomy reversal
  • sperm retrieval from testes.
  • assisted reproduction