Obstretrics Pt. 2 Flashcards

1
Q

Why is prenatal diagnostic testing performed?

A
  • Usually performed if there is suspicion of disease in the foetus, for example:
    • Family history
    • Past obstetric history (RhD alloimmunisation)
    • Serum screening tests
    • Ultrasound scanning (12 week dating or 20 week anomaly)
  • Prenatal diagnosis often happens after some form of screening test
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2
Q

What are the attributes of a screening test?

A
  • Relevance of the disease
  • Effect of early diagnosis on management (e.g. offering termination)
  • Sensitivity
  • Specificity
  • Predictive value
  • Affordability
  • Equity (available to all)
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3
Q

What are different types of prenatal diagnostic tests?

A
  • Ultrasound diagnosis
  • Invasive test- CVS or amniocentesis
  • Invasive test- cordocentesis
  • Ultrasound then invasive test
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4
Q

What conditions are diagnosed with ultrasound?

A
  • Neural tube defect
  • Gastroschisis
  • Cystic adenomatoid malformation of lung
  • Twin to twin transfusion syndrome
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5
Q

What conditions are diagnosed with CVS or amniocentesis?

A
  • Downs syndrome
  • Thalassaemia
  • Cystic Fibrosis
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6
Q

What conditions are diagnosed with cordocentesis?

A
  • Alloimmune thrombocytopaenia
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7
Q

What conditions are diagnosed with ultrasound first then invasive test?

A
  • Congenital diaphragmatic hernia
  • Exomphalos
  • Ventriculomegaly
  • Duodenal atresia
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8
Q

What does it mean when a woman initially has no IgM or IgG for a particular virus early in pregnancy but develops IgM or IgG later on?

A
  • Had a clinical or subclinical infection with virus at some point during pregnancy
  • This is usually only done if there are ultrasound results suggestive of infection or if there is a history of exposure to a particular virus
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9
Q

Describe cell-free foetal DNA (cffDNA)?

A
  • Extracted from the maternal blood
  • Uses
    • Determination of foetal blood group in cases of RhD alloimmunisation
    • Determine the sex of the foetus in X-linked disorders
    • Diagnose skeletal dysplasias (e.g. achondroplasia)
  • The levels of cffDNA increases with gestation, however, it decreases to undetectable levels by the first day after birth
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10
Q

What are the two most common invasive tests for prenatal diagnosis?

A
  • Amnioncentesis and Chorion Villous Sampling are the two MOST COMMON invasive tests that are used to check the karyotype of the foetus or diagnose single gene disorders
  • These tests carry a small but significant risk of miscarriage
  • So, the seriousness of the condition should be enough to warrant the risk
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11
Q

What are three options usually available following results of a prenatal test?

A
  • Continue
    • May facilitate care around the time of delivery and may help the mother/partner prepare for the birth of a baby with a serious condition
  • Termination of pregnancy
  • Terminate, but provide information which may prove useful when counselling about recurrence risks in future pregnancies
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12
Q

What cells are sampled Chorion Villous Sampling? (Chorion Villous Biopsy)
How is CVS done?

A
  • Foetal trophoblast cells in the mesenchyme of the villi divide rapidly in the first trimester
  • CVS aims to take a sample of these rapidly dividing cells from the developing placenta
  • This can either be done by:
    • Passing a needle under ultrasound guidance through the abdominal wall and myometrium into the placenta
    • Passing a fine catheter (or biopsy forceps) through the cervix into the placenta
  • The laboratory can check the sample for aneuploidy
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13
Q

Why should the woman be ultrasound scanned initially before CVS?

A
  • To confirm that the pregnancy is viable before the CVS
  • To ensure that it is a singleton pregnancy (prenatal diagnosis in multiple pregnancy is more complicated)
  • To confirm gestational age (CVS should NOT be performed < 10 weeks gestation)
  • To localise the placenta and determine whether a transabdominal or transcervical approach is more appropriate
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14
Q

Which type of CVS is most commonly performed? (Transabdominal or transcervical)

A
  • Transabdominal
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15
Q

What is the additional risk of miscarriage with CVS?

A
  • 2%
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16
Q

What is placental mosaicism?

A
  • Is sometimes found where two different cell types are found in the same sample (one cell line is normal and the other is abnormal)
  • This pattern may be present in the placenta and NOT the foetus (confined placental mosaicism)
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17
Q

What is amniocentesis?

A
  • Amniotic fluid contains amniocytes and fibroblasts shed from foetal membranes, skin and the foetal genitourinary tract
  • Amniocentesis takes a sample of 15-20 mL of amniotic fluid containing these cells
  • It is done by passing a needle under continuous direct ultrasound through the abdominal wall and myometrium into the amniotic cavity and aspirating fluid
  • The total post-amniocentesis pregnancy loss risk = 1.9% (if performed > 15 weeks)
  • Laboratories can provide a result for common aneuploidies (T21, 18, 13, X and Y) within 48 hours
  • Full culture takes around 7-10 days
  • Amniotic fluid can also be used to check for foetal viral infections
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18
Q

What is the advantage of CVS over amniocentesis?

A
  • CVS can be performed earlier in the pregnancy
  • This is at a stage where surgical termination of pregnancy is possible
  • CVS also provides a larger sample of DNA
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19
Q

What is Cordocentesis?
What is the most common reason for it?
How does it work?

A
  • This is performed when foetal blood is needed
  • The MOST COMMON reason for cordocentesis is:
    • Suspected severe foetal anaemia
    • Thrombocytopaenia
  • A needle is passed under ultrasound guidance through the abdominal wall and myometrium into the umbilical cord at the point where it insert into the placenta
  • Can be performed from about 20 weeks
  • Risk of miscarriage varies with indication and position of the placenta
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20
Q

Describe the prenatal diagnosis of Downs Syndrome?

A
  • The screening test involves a combination of:
    • Nuchal translucency (NT)
      • Thicker in foetuses with Down syndrome
    • Crown-rump length (CRL) from 11+2 to 14+1 weeks
    • Maternal blood test showing hCG and PAPP-A levels from 10 - 14+1 weeks
  • The mother’s age is also taken into account when determining risk
  • A quadruple test (hCG, AFP, unconjugated oestriol and inhibin A) is the screening strategy of choice in the 2nd trimester
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21
Q

Describe Prenatal Diagnosis of Foetal Single Gene Disorders

When are prenatal tests offered?

A
  • Certain autosomal dominant single gene disorders can be diagnosed antenatally
  • Offered when:
    • Father is known to be affected
    • Risk of recurrence
    • Condition is suspected on ultrasound:
      • E.g. autosomal dominant severe skeletal dysplasia (achondroplasia, thanatophoric dysplasia)
        • These are caused by a mutation in FGFR3
        • PCR can be done to identify the FGFR3 mutation in cffDNA
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22
Q

Describe Foetal Blood Group test

A
  • If RhD-positive DNA is amplified from the blood of an RhD-negative woman, it must have come from the foetus (thereby showing that the foetus is RhD-positive)
  • This test is used in RhD-negative mothers with anti-D antibodies to determine the blood group of the foetus
    • If the foetus is RhD-positive, it is at risk of alloimmune haemolytic disease
  • Foetal blood group can be determined from samples taken in the first trimester
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23
Q

What are common musculoskeletal antenatal obstretric complications

A
  • Backache
  • Symphysis Pubic Dysfunction
  • Carpal Tunnel Syndrome
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24
Q

As an antenatal obstetric complication, what is backache caused by and what are its complications?

How to manage backache?

A
  • Very common
  • Caused by:
    • Hormone induced laxity of the spinal ligaments
    • Shifting in the centre of gravity as the uterus grows
    • Additional weight gain
  • Causes exaggerated lumbar lordosis
  • Advise correct posture, avoid lifting heavy objects, avoid high-heels, regular physiotherapy and simple analgesia (paracetamol or co-codamol)
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25
Q

What is Symphysis Pubic Dysfunction?

A
  • Excruciatingly painful usually occurring in the 3rd trimester
  • The symphysis pubis becomes loose causing the two halves of the pelvis to rub against each other when walking or moving
  • Improves after delivery
  • Management involves simple analgesia
  • A low stability belt may help
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26
Q

What is Carpal Tunnel Syndrome?
What are the symptoms?
How is it managed?

A
  • Compression neuropathies occur due to increased soft tissue swelling
  • The median nerve is compressed as it passes through the carpal tunnel
  • Symptoms include numbness, tingling and weakness of the thumb and forefinger and often severe pain at night
  • Simple analgesia and splinting of the affected hand can help
  • Surgical decompression is rarely performed in pregnancy
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27
Q

What are common gastrointestinal antenatal obstretric complications?

A
  • Constipation
  • Hyperemesis gravidarum
  • Gastro-oesophageal reflux
  • Haemorrhoids
  • Obstretric cholestasis
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28
Q

Describe constipation (antenatal obstretric complication)

A
  • COMMON
  • Usually results from a combination of hormonal and mechanical factors that slow gut motility
  • Women should be reassured and given advice regarding adopting a high-fibre diet
  • Medications are best avoided if possible
  • Mild (non-stimulant) laxatives such as lactulose may be suggested
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29
Q

What is hyperemesis gravidarum?

A
  • Hyperemesis gravidarum is a severe, intractable form of nausea and vomiting
  • The likely cause is multifactorial
  • Nausea and vomiting in pregnancy is extremely common
  • The symptoms are usually most pronounced in the first trimester
  • Most cases of nausea and vomiting in pregnancy are mild and self-limiting
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30
Q

What are the consequences of hyperemesis gravidarum?

A
  • Electrolyte imbalances
  • Disturbs nutritional intake and metabolism
  • Physical and psychological debilitation
  • Adverse pregnancy outcome (increased risk of preterm birth and LBW)
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31
Q

What can severe cases of hyperemesis gravidarum cause?

A
  • Malnutrition
  • Vitamin deficiencies (e.g. Wernicke’s encephalopathy)
  • Intractable retching can lead to Mallory Weiss tears
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32
Q

What is general treatment of hyperemesis gravidarum?

A
  • Fluid replacement
  • Thiamine supplementation
  • Antiemetics (e.g. phenothiazines)
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33
Q

How is hyperemesis gravidarum diagnosed?
How is severity assessed?
How is it managed?
(RCOG Green Top Guidelines)

A
  • Diagnosed when there is a triad of:
    • More than 5% pre-pregnancy weight loss
    • Dehydration
    • Electrolyte imbalance
  • Severity should be assessed using Pregnancy-Unique Quantification of Emesis (PUQE)
  • Mild
    • Use antiemetics in the community
    • Ambulatory day care management can be used if primary care fails and PUQE score < 13
  • Consider inpatient treatment if:
    • Continued N/V and can’t keep down oral antiemetics
    • Continued N/V + ketonuria and/or weight loss (> 5% body weight) despite oral antiemetics
    • Confirmed or suspected comorbidity (e.g. UTI) and inability to tolerate oral antibiotics
  • Antiemetics
    • Antihistamines (e.g. cyclizine) and phenothiazines (e.g. promethazine) should be used as first-line
      • Second-line: metoclopramide, ondansetron
    • Combinations can be used if women fail to respond to a single agent
    • Parenteral or rectal route if oral is not tolerated
    • WARNING: extra-pyramidal side-effects and oculogyric crises can occur with phenothiazines and metoclopramide
  • Rehydration and Correction of Electrolyte Imbalance
    • Normal saline with additional potassium chloride in each bag, with administration guided by monitoring of electrolytes
    • Check urea and electrolytes daily
    • Thiamine supplementation should be given to all women admitted with prolonged vomiting
    • Women who are admitted should also be offered thromboprophylaxis with LMWH
  • Alternative therapy
    • Ginger, acupressure and hypnosis are alternative options
  • MDT
  • Discharge
    • Individualised management plan
    • If symptoms continue into second and third trimester, should offer serial scans to monitor foetal growth
    • Advise about a risk of recurrence in future pregnancies
  • Other
    • Assess mental health status (refer to psychological support if necessary)
    • Advise adequate resting
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34
Q

Describe gastro-oesophageal reflux (antenatal obstretric complication)

A
  • VERY COMMON
  • Weight effect of pregnant uterus and hormonally induced relaxation of the oesophageal sphincter leads to reflux
  • Lifestyle modification (e.g. smoking cessation, frequent light meals and lying with the head propped up at night) are usually helpful
  • If this is insufficient, antacids, histamine inhibitors and PPIs can be used
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35
Q

Why are haemorrhoids more common in pregnancy?

How can they be managed?

A
  • This is more common during pregnancy due to the effects of circulating progesterone on the vasculature, pressure on the superior rectal veins by the gravid uterus and increasing circulating volume
  • Conservative measures are usually taken such as local anaesthetic/anti-irritant creams and a high-fibre diet
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36
Q

What is Obstretric Cholestasis?

A
  • Also known as intrahepatic cholestasis of pregnancy
  • Normally presents in the second half of pregnancy with pruritus and abnormal LFTs without an alternative cause
  • This is associated with an increased risk of spontaneous preterm birth, iatrogenic preterm birth and foetal death
  • The pruritus can affect sleep
  • Normally treated with ursodeoxycholic acid which improves pruritus and liver function but has no effect on maternal or foetal outcome
  • Women with obstetric cholestasis are offered delivery after 37 weeks
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37
Q

Describe varicose veins in pregnancy
What are potential causes and complications of varicose veins?
How can you manage varicose veins?

A
  • May occur for the first time in pregnancy or pre-existing veins may become worse
  • Maybe due to relaxant effect of progesterone on vascular smooth muscle
  • Weight of the pregnant uterus can also contribute
  • Conservative measures include support stockings, avoid standing for long periods of time and simple analgesia
  • Thrombophlebitis may occur in a large varicose vein
  • A large superficial varicose vein may bleed profusely
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38
Q

Describe oedema in pregnancy

A
  • COMMON
  • There is generalised soft-tissue swelling and increased capillary permeability, allowing intravascular fluid to leak into the extravascular compartment
  • Fingers, toes and ankles are often worst affected
  • Exacerbated by hot weather
  • Best dealt with by frequently resting ad elevating the legs
  • Sometimes, support stockings are indicated
  • Rings and jewellery may need to be removed
  • IMPORTANT: generalised (rather than lower limb) oedema may be a feature of pre-eclampsia so it is important to check blood pressure and urine for protein
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39
Q

What are other minor disorders of pregnancy?

A
  • Itching
  • Urinary incontinence
  • Nosebleeds
  • Thrush
  • Headache
  • Fainting
  • Breast soreness
  • Tiredness
  • Altered taste
  • Insomnia
  • Leg cramps
  • Striae gravidarum and chloasma (skin discoloration)
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40
Q

What are fibroids?

A
  • These are compact masses of smooth muscle found:
    • In the cavity of the uterus (submucous)
    • Within the uterine muscle (intramural)
    • On the outside surface of the uterus (subserous)
  • They may enlarge in pregnancy causing problems later in pregnancy or during delivery (e.g. a large fibroid near the cervix and may obstruct vaginal delivery)
  • A subserous pedunculated fibroid can tort
    • This can also cause acute abdominal pain and tenderness (and hence present very similarly to red degeneration)
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41
Q

What is one of the most common complications of fibroids in pregnancy and what is its treatment?

A
  • Red degeneration
  • As it grows, the fibroid can become ischaemic
  • This manifests as acute pain, tenderness over the fibroid and vomiting
  • If severe, it can precipitate uterine contractions causing miscarriage or preterm labour
  • This requires treatment with potent analgesics (opiates) and IV fluids
  • Symptoms usually settle after a few days
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42
Q

What is the differential diagnosis for red degeneration?

A
  • Acute appendicitis
  • Pyelonephritis/UTI
  • Ovarian cyst accident
  • Placental abruption
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43
Q

What is used to diagnose fibroids and red degeneration?

A
  • History and ultrasound scanning is used to diagnose both conditions
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44
Q

Describe retroversion of the Uterus

A
  • 15% of women have a retroverted uterus
  • Most of the time, as the uterus grows through pregnancy, a retroverted uterus would flip out of the pelvis and begin to fill the abdominal cavity (as an anteverted uterus would)
  • Occasionally, the uterus remains retroverted as it grows and it will eventually fill up the entire pelvic cavity
  • This leads to stretching of the base of the bladder and the urethra
  • This can lead to urinary retention (usually at 12-14 weeks)
  • This is painful and can cause long-term bladder damage
  • Catheterisation is essential until the position of the uterus has changed
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45
Q

What are some congenital uterine abnormalities?

A
  • The shape of the uterus is embryologically determined by fusion of the Mullerian ducts
  • Abnormalities of fusion can lead to several anomalies such as:
    • Subseptate Uterus
    • Bicornuate uterus (deep indentation at the fundus of the uterus)
    • Uterus didelphys
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46
Q

What are associated problems with a Bicornuate uterus?

A
  • Miscarriage
  • Preterm labour
  • Preterm premature rupture of membranes
  • Abnormalities of lie and presentation
  • Higher C-section rate
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47
Q

Describe Ovarian cysts in pregnancy

A
  • COMMON
  • Malignancy is uncommon
  • Most common pathological ovarian cyst:
    • Serous cyst
    • Benign teratoma
  • Physiological cysts of the corpus luteum may grow to several centimetres but rarely require treatment
  • Asymptomatic cysts may be followed up by clinical/ultrasound examination
  • Large cysts may require surgery
    • Surgery is usually postponed until the late 2nd/early 3rd trimester (this means that the baby could survive if it had to be delivered)
  • Symptomatic cysts usually require an EMERGENCY laparotomy and ovarian cystectomy or may be an oophorectomy
  • Full assessment includes a family history of ovarian or breast malignancy, tumour markers and ultrasound investigation of both ovaries
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48
Q

What are major problems with ovarian cysts in pregnancy?

A
  • Large cysts could undergo torsion, haemorrhage or rupture
  • This causes acute abdominal pain
  • The pain and inflammation may result in miscarriage or preterm labour
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49
Q

Describe cervical cancer in pregnancy and how does it present?

A
  • The cervix is more difficult to visualise using colposcopy in pregnancy
  • Cervical cancer is often asymptomatic or may present with vaginal bleeding (especially post-coital)
  • The diagnosis of cervical cancer in pregnancy raises difficult questions about termination of pregnancy
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50
Q

What is a urinary tract infection?
What is a UTI associated with?
What are predisposing factors?

A
  • > 105 colony forming units/mL in urine culture
  • UTI and pyelonephritis are associated with LBW and preterm delivery
  • Predisposing factors:
    • History of recurrent cystitis
    • Renal tract abnormalities (e.g. duplex system, scarred kidneys, ureteric damage and stones)
    • Diabetes mellitus
    • Bladder emptying problems (e.g. multiple sclerosis)
  • The classic UTI presentation of frequency, dysuria and haematuria are rarely seen
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51
Q

What do you see O/E for a UTI?

A
  • tachycardia, pyrexia, dehydration and loin tenderness may be present
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52
Q

What are the investigations for a UTI?

A
  • FBC

- MSU

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53
Q

What is the management of a UTI?

A
  • If there is strong suspicion of UTI< treatment with antibiotics should be started straight away
  • Encourage plentiful fluid intake
  • Use simple analgesics (e.g. paracetamol)
  • First-line antibiotic: amoxicillin or oral cephalosporins
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54
Q

What are the organisms responsible for a UTI?

A
  • MOST COMMON organism is E. coli
  • Other organisms:
    • Proteus
    • Pseudomonas
    • Klebsiella
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55
Q

What signs is pyelonephritis characterised by?

A
  • Dehydration
  • Very high temperature
  • Systemic disturbance
  • Shock (occasionally)
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56
Q

What is the management of pyelonephritis?

A
  • IV fluids
  • Opiate analgesia
  • IV antibiotics (cephalosporins or gentamicin)
  • Check renal function (baseline urea and electrolytes)
  • Monitor baby with CTG
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57
Q

What should happen if there are recurrent UTIs in pregnancy?

A
  • MSU specimens should be sent to microbiology at each antenatal visit
  • Low-dose prophylactic oral antibiotics
  • Further investigations should be delayed until after delivery (unless serious symptoms (e.g. frank haematuria) suggest that urgent diagnosis is necessary)
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58
Q

What investigations should be done for recurrent UTIs in pregnancy?

A
  • Renal ultrasound
  • DMSA scan
  • Creatinine clearance
  • IV urogram
  • Cystoscopy
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59
Q

Describe VTE in pregnancy

Why is pregnancy a hypercoagulable state?

A
  • MOST COMMON cause of direct maternal death in the UK
  • Pregnancy is a hypercoagulable state because of an alteration in the thrombotic and fibrinolytic systems
    • Increase in factors 8, 9, 10 and fibrinogen
    • Decrease in protein C and antithrombin-III
  • These changes are thought to be evolutionary in order to reduce the risk of haemorrhage following delivery
  • The weight of the gravid uterus places pressure on the IVC leading to venous stasis, thereby further increasing the risk of thromboembolism
  • Immobility also contributes to VTE risk
  • Pregnancy is associated with a 6-10 fold increase in VTE risk
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60
Q

What are the risk factors of getting a VTE in pregnancy?

A
  • Pre-existing
    • maternal age (> 35 years)
    • thrombophilia
    • obesity (> 80kg)
    • previous thromboembolism
    • severe varicose veins
    • smoking
    • malignancy
  • Specific to pregnancy
    • Multiple gestation
    • Pre-eclampsia
    • Grand multiparity
    • C-section
    • Sepsis
    • Prolonged bed rest
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61
Q

What are the hereditary forms of thrombophilia?
What is acquired thrombophilia associated with?
What is APS?

A
  • Some changes in the coagulation/fibrinolytic system may be inherited or acquired
  • Main hereditary forms of thrombophilia
    • Protein C deficiency
    • Protein S deficiency
    • AT-III deficiency
    • Factor V Leiden
    • Prothrombin mutation G20210A
  • Heritable thrombophilias are present in 15% of the Western population
  • Acquired thrombophilia is most commonly associated with anti-phospholipid syndrome (APS)
  • APS is the combination of lupus anticoagulant with or without anticardiolipin antibodies, with a history of recurrent miscarriage and/or thrombosis
  • It may be associated with SLE
  • Women with a history of thrombotic events should be screened for thrombophilia
  • If thrombophilia is present, thromboprophylaxis should be considered
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62
Q

What is the diagnosis of acute DVT?

A
  • Usually presents with calf pain with redness and swelling (and tender)
  • NOTE: women’s legs often swell during pregnancy so unilateral symptoms should ring alarm bells
  • Check for symptoms of PE
  • Compression ultrasound is the first investigation used in suspected DVT
  • NOTE: a thrombus that is confined to the calf veins is unlikely to lead to a PE
  • Venography is invasive (requires contrast injection and use of X-rays) but allows excellent visualisation of veins above and below the knee
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63
Q

What is the diagnosis of acute PE?

A
  • Usually presents with mild SOB or inspiratory chest pain
  • The woman may be slightly tachycardic with mild pyrexia
  • More rarely, massive PE could cause sudden cardiorespiratory collapse
  • If suspected, ECG, CXR and ABG should be performed to exclude other diagnoses
  • You may investigate the presence of DVT using ultrasound
  • If PE is strongly suspected, a VQ scan or a CTPA may be performed
  • NOTE: D-dimer levels are physiologically elevated in pregnancy
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64
Q

What is the treatment of acute VTE?

A
  • Warfarin is contraindicated in pregnancy (except in women with mechanical heart valves) because it crosses the placenta and can cause limb and facial defects and foetal intracerebral haemorrhage
  • LMWH is the treatment of choice
  • They do NOT cross the placenta and it is easy to administer
  • After delivery, women can choose to change to warfarin or remain on LMWH
  • Graduated elastic stockings should be used for the initial treatment of DVT and should be worn for 2 years after DVT to prevent post-thrombotic syndrome
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65
Q

What is the management of Acute VTE (RCOG Green Top Guidelines)?

A
  • Treatment with LMWH (until the diagnosis is excluded)
  • The therapeutic dose should be calculated based on the woman’s booking or early pregnancy weight
  • DVT
    • Compression duplex ultrasound should be performed if there is clinical suspicion of DVT
      • If negative and low clinical suspicion - stop anticoagulants
      • If negative and high clinical suspicion - stop anticoagulants and repeat ultrasound on days 3 and 7
    • Initial management includes elevating the leg and applying a graduated elastic stocking
  • PE
    • Perform ECG and CXR
      • If the CXR is abnormal and there is clinical suspicion of PE, a CTPA should be performed in preference to a VQ scan
    • If they also have symptoms of DVT, compression duplex ultrasound should be performed
    • If they have NO symptoms of DVT, a VQ scan or CTPA should be performed
    • Alternative or repeat testing should be carried out if the VQ scan and CTPA are normal but the clinical suspicion of PE remains
    • Anticoagulant treatment should be continued until PE is definitively excluded
    • VQ scanning has a higher risk of childhood cancer, but CTPA has a higher risk of maternal breast cancer (BUT, the absolute risk is very small)
    • NOTE: IVC filters may be considered in the peripartum period for patients with iliac vein VTE or in patients with proven DVT and those who have recurrent PE despite anticoagulation
    • Massive PE
      • Options include IV unfractionated heparin, thrombolytic therapy, thoracotomy or surgical embolectomy
      • IV unfractionated heparin preferred when cardiovascular compromise
      • Urgent portable echocardiogram or CTPA should be arranged
      • If massive PE is confirmed, immediate thrombolysis should be considered
    • Maintenance Treatment of VTE
      • Treatment with therapeutic doses of subcutaneous LMWH should be continued for the remainder of the pregnancy and for at least 6 weeks posnatally and until at least 3 months of treatment in total
    • Women should be taught to self-inject
    • Watch out for heparin-induced thrombocytopaenia and heparin allergy
    • Women should be offered a choice of LMWH or oral anticoagulant (this requires routine INR monitoring)
    • NOACs may be used in patients who cannot tolerate heparin
    • NOTE: neither heparin nor warfarin are contraindicated in breastfeeding
    • Anticoagulation during labour and delivery
      • If VTE occurs at term, IV unfractionated heparin should be considered
      • If a woman on LMWH maintenance therapy goes into labour, they should NOT inject any more
      • If delivery is planned, LMWH should be discontinued 24 hours before
      • Regional anaesthetic (e.g. epidural) should not be undertaken until at least 24 hours after the last dose of LMWH
      • LMWH should not be given until 4 hours after the use of spinal anaesthesia or after the epidural catheter has been removed
      • Women who are at HIGH RISK OF HAEMORRHAGE who require continuous heparin should be managed with IV unfractionated heparin
    • Prevention of Post-Thrombotic Syndrome
      • Prolonged use of LMWH (> 12 weeks) is associated with lower risk of post-thrombotic syndrome
      • Graduated elastic compression stockings also reducer risk
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66
Q

How does alcohol affect pregnancy?

A
  • > 1 pint per day = FGR
  • Foetal alcohol syndrome
  • Foetal alcohol syndrome is not seen consistently in women who are heavy consumers of alcohol (there appears to be some difference in the susceptibility of foetuses to foetal alcohol syndrome)
  • May have to involve social workers
  • May have to arrange formal psychiatric/addiction assessment
  • Markers of acute alcohol abuse like MCV and GGT are not reliable in pregnancy
  • Malnutrition and required vitamin B and iron supplementatio
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67
Q

How does smoking affect the placenta?

What is smoking associated with?

A
  • Smoking acutely reduces placental perfusion
  • It is associated with:
    • Increased perinatal mortality
    • Smaller babies
    • Higher risk of placental abruption
  • Quitting by 15 weeks gestation reduces the risk as much as quitting before pregnancy
  • ALL women should be counselled regarding smoking cessation at the booking visit
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68
Q

What is amniotic fluid?

A
  • Almost exclusively comes from foetal urine from the 2nd trimester onwards
  • Roles
    • Protection from pressure or trauma
    • Allows limb movement
    • Permits foetal lungs to expand and develop through breathing
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69
Q

What is oligohydramnios?

A
  • Commonly defined as amniotic fluid index (AFI) < 5th centile for gestation
  • AFI is an ultrasound estimation of amniotic fluid volume
  • May be suspected if there is a history of clear fluid leaking from the vagina
  • On palpation of the abdomen, the foetal poles may be very obvious and hard with a small for dates uterus
  • Prognosis depends on cause of oligohydramnios
  • In severe early-onset oligohydramnios, pulmonary hypoplasia and limb deformities are common
  • Renal agenesis (Potter syndrome) and bilateral multicystic kidneys carry a LETHAL prognosis because life is impossible without functioning kidneys
  • Oligohydramnios due to FGR/utereroplacental insufficiency tends to be less severe
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70
Q

What are the causes of oligohydramnios?

A
  • Renal agenesis (Ultrasound: no kidneys or bladder)|
  • Multicystic kidneys (Ultrasound: enlarged kidneys with multiple cysts, no visible bladder)
  • Urinary tract abnormality/obstruction (Ultrasound: kidneys may be present but urinary tract dilatation)
  • FGR and placental insufficiency (Clinical: reduced SFH, reduced foetal movements, possibly abnormal CTG, Ultrasound: FGR, abnormal fetal Doppler wave forms)
  • Maternal drugs e.g. NSAIDs (Withdrawing NSAIDs causes amniotic fluid to accumulate)
  • PPROM (Leakage) diagnosed by speculum examination: pool of amniotic fluid on posterior blade
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71
Q

What is polyhydramnios?

What does it present with?

A
  • Commonly defined as AFI > 95th centile for gestation
  • May present with severe abdominal swelling and discomfort
  • The abdomen may appear distended out of proportion with the woman’s gestation
  • The abdomen may be tense and tender, and the foetal poles will be difficult to palpate
  • Polyhydramnios that may be caused by maternal diabetes will correct itself once glycaemic control is optimised
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72
Q

What is the management of polyhydramnios?

A
  • Identifying the cause
  • Relieving discomfort (e.g. amniodrainage)
  • Assessing the risk of preterm labour due to uterine overdistension
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73
Q

What are the three type of breech presentations?

A
  • Extended (frank) breech (MOST COMMON)
  • Flexed (complete) breech
  • Footling breech
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74
Q

What are predisposing factors for breech presentation?

A
  • Maternal
    • Fibroids
    • Congenital uterine abnormalities (e.g. bicornuate uterus)
    • Uterine surgery
  • Foetal
    • Multiple gestation
    • Prematurity
    • Placenta praevia
    • Abnormality (e.g. anencephaly, hydrocephalus)
    • Foetal neuromuscular condition
    • Oligo/polyhydramnios
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75
Q

What is the management of breech (RCOG Green Top Guidelines)?

A
  • If Breech at or after 36 weeks = confirm with ultrasound
  • This should look at foetal biometry, amniotic fluid volume, placental site and position of the foetal legs
  • If breech:
    • External cephalic version
    • Vaginal breech delivery
    • Elective Caesarean section
  • Planned vaginal delivery of a breech linked to 3% increased risk of death or serious morbidity to the baby
  • The BEST METHOD of delivering breech singleton is by planned Caesarean section
  • Planned C-section for breech at term carries a small risk of increased maternal complications
  • Rate of maternal complications are lowest for successful vaginal birth and higher for planned C-section
  • BUT the risks are highest with emergency C-section which is needed in about 40% of planned vaginal breech deliveries
  • Women should be informed about the risks of C-section:
    • Risks of opting for vaginal birth after C-section
    • Increased risk of complications at repeat C-sections
    • Risk of an abnormally invasive placenta
  • C-sections are associated with a small increase in risk of stillbirth for subsequent babies (but this may not be causal)
  • If a woman presents with an unplanned breech presentation in labour, offering planned C-section depends on the stage of labour (women near or in active second stage of labour should NOT routinely be offered C-section)
  • Induction of labour is NOT usually recommended
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76
Q

What are the features of HIGH RISK planned vaginal breech?

A
  • Hyperextended neck on ultrasound
  • High estimated foetal weight
  • Low estimated weight
  • Footling presentation
  • Evidence of antenatal foetal compromise
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77
Q

What is external cephalic version?

A
  • This is technique that reduces the number of C-sections due to breech presentations
  • Success rates vary depending on the experience of the operator (but is around 50%)
  • Performed at or after 37 weeks gestation
  • Should be performed with a tocolytic (prevents contractions e.g. nifedipine)
  • Woman is laid flat
  • The obstetrician uses their hands to make the baby do a forward role thereby correcting the breech position
  • Foetal heart rate should be monitored before and after the procedure
  • Anti-D should be administered if the woman is Rhesus-negative
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78
Q

What are the contraindications of external cephalic version?

A
  • Foetal abnormality (e.g. hydrocephalus)
  • Placenta praevia
  • Oligo/polyhydramnios
  • History of antepartum haemorrhage
  • Previous C-section or myomectomy scar on the uterus
  • Multiple gestation
  • Pre-eclampsia or hypertension
  • Plan to deliver by C-section anyway
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79
Q

What are the risks of external cephalic version?

A
  • Placental abruption
  • Premature rupture of membranes
  • Cord accident
  • Transplacental haemorrhage (hence why anti-D is important in Rhesus-negative women)
  • Foetal bradycardia
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80
Q

Describe vaginal breech delivery technique

A
  • Delivery of the Buttocks
    • Most of the time, full dilatation and descent of the breech will have occurred naturally
    • The buttocks will lie in the anterior-posterior diameter
    • An episiotomy can be cut once the anterior buttock is delivered and the anus is seen over the fourchette (frenulum of labia minora)
  • Delivery of Legs and lower body
    • If the legs are flexed, they will deliver spontaneously
    • If extended, they may need to be delivered with Pinard’s manoeuvre
    • This involves using a finger to flex the leg at the knee and extend the hip, first anteriorly then posteriorly
    • Maternal effort and contractions help
  • Delivery of the Shoulders
    • The baby is initially lying with the shoulders in the transverse diameter of the pelvic midcavity
    • As the anterior shoulder rotates into the anterior-posterior diameter, the spine or the scapula will become visible
    • A finger can then be placed gently above the shoulder to help deliver the arm
    • As the posterior arm reaches the pelvic floor, it will rotate anteriorly
    • Once the spine becomes visible, the second arm will be delivered
    • Loveset’s manoeuvre copies these natural movements
  • Loveset’s manoeuvre is unnecessary to do routinely
  • Delivery of the Head
    • Delivered using Mauriceau-Smellie-Veit Manoeuvre
    • The baby lies on the obstetrician’s arm with downward traction on the head via a finger in the mouth and one on each maxilla
    • Delivery occurs with first downward then upward movement
    • Forceps may be used if this manoeuvre is difficult
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81
Q

What are complications of vaginal breech delivery?

A
  • The baby getting stuck

- Inappropriate use of oxytocic agents and trying to pull the baby out will increase the risk of obstruction

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82
Q

What are some other foetal malpresentations?

A
  • Transverse lie (usually results in shoulder presentation)
  • Oblique lie
  • These women are at risk of cord prolapse following spontaneous rupture of membranes
  • They are also at risk of prolapse of the hand, shoulder or foot once in labour
  • In most cases, the woman is multiparous with a lax uterus and abdominal wall musculature
  • Gentle version of the baby’s head will restore the presentation to cephalic
  • In these women, the abdomen may appear asymmetrical
  • On palpation, the foetal head or buttocks may be in the iliac fossa
  • Palpation over the pelvic brim may reveal an empty pelvis
  • A woman in labour with a baby who’s lie is anything other than longitudinal will NOT be able to deliver vaginally
  • C-section is required - if it is NOT performed, the baby and the mother are at considerable risk of morbidity and mortality
    • EXCEPTION: preterm/small babies
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83
Q

What is post-term pregnancy?
What are risks of post-term pregnancy?
How can risks be reduced?
When should immediate induction of labour take place?

A
  • Defined as a pregnancy that has extended to or beyond 42 weeks gestation
  • This affects 10% of pregnancies
  • Associated with increased risk to both foetus and mother such as:
    • Stillbirth
    • Perinatal death
    • Prolonged labour
    • C-section
  • Foetal surveillance and induced labour are two strategies to reduce risk
  • CTG should be performed at and after 42 weeks
  • Ultrasound can help assess amniotic fluid volume and foetal growth rate
  • IMMEDIATE induction of labour should take place if:
    • Reduced amniotic fluid on ultrasound
    • Foetal growth is reduced
    • Reduced foetal movements
    • CTG is not perfect
    • Mother is hypertensive or suffers from a significant medical condition
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84
Q

Describe vaginal bleeding in pregnancy

A
  • COMMON but causes anxiety
  • Vaginal bleeding:
    • < 24 weeks is defined as a threatened miscarriage
    • 24+ weeks is defined as antepartum haemorrhage (APH)
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85
Q

What are the causes of Antepartum Haemorrhage (3% of pregnancies)?

A
  • Placental
    • Placental abruption
    • Placenta praevia
    • Vasa praevia
  • Local Causes
    • Cervicitis
    • Cervical ectropion
    • Cervical carcinoma
    • Vaginal trauma
    • Vaginal infection
  • NOTE: of the 3%, 1% is caused by placental abruption, 1% by placenta praevia and the remaining 1% from the other causes
  • APH must ALWAYS be taken seriously
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86
Q

What would you state in a history for vaginal bleeding?

A
  • How much bleeding?
  • Triggering factors (e.g. post-coital?)
  • Associated with pain or contractions?
  • Is the baby moving?
  • Last cervical smear (date/normal or abnormal)
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87
Q

How would you examine a pregnant woman with vaginal bleeding?

A
  • Pulse, BP
  • Is the uterus soft or tender and firm?
  • Foetal heart auscultation/CTG
  • Speculum vaginal examination
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88
Q

What investigations would you do for vaginal bleeding?

A
  • Depends on degree of bleeding - FBC, clotting and cross-match 6 units of blood (if praevia or abruption)
  • Ultrasound - assess foetal size, presentation, amniotic fluid, placental fluid and morphology
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89
Q

Describe Rhesus antigens

A
  • There are at least 40 Rhesus antigens and the most clinically important are C, D and E
  • They are coded on two adjacent genes on chromosome 1
    • One gene encodes C/c and E/e
    • The other codes for D (Rhesus antigen)
  • In practice, only anti-D (mostly) and anti-c (rarely) cause haemolytic disease of the foetus and newborn (HDFN)
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90
Q

How does HDFN from rhesus isoimmunisation occur?

A
  • A rhesus-negative mother must conceive a baby who has inherited the rhesus-positive phenotype from the father
  • Foetal cells must gain access to the maternal circulation in a sufficient volume to provoke a maternal antibody response
  • Maternal antibodies must cross the placenta and cause immune destruction of red cells in the foetus
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91
Q

Why doesn’t Rhesus disease affect the first pregnancy?

A
  • Rhesus disease does NOT affect the first pregnancy because the primary immune response is usually weak and consists mainly of IgM which does NOT cross the placenta
  • In a subsequent pregnancy with a Rhesus-positive foetus, Rhesus-positive cells pass from the baby to the mother and cause resensitisation
  • Then, B cells produce a much larger response with IgG antibodies that can cross the placenta into the foetal circulation
  • This can lead to severe anaemia due to haemolysis and the foetus may die unless transfusion is performed
  • RhD-negativity is present in 15% of the Caucasian population in the UK (and is lower in all other ethnic groups)
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92
Q

What are potential sensitising events for rhesus disease?

A
  • Miscarriage
  • Termination of pregnancy
  • Antepartum haemorrhage
  • Invasive prenatal testing (CVS, amniocentesis, cordocentesis)
  • Delivery
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93
Q

How do you prevent Rhesus isoimmunisation?

A
  • Rhesus isoimmunisation can be prevented by administration of IM anti-D immunoglobulin to the mother
  • This ‘mops up’ circulating Rhesus-positive cells before an immune response is elicited in the mother
  • Anti-D immunoglobulin should be administered ASAP after a potential sensitising event (ideally within 72 hours of exposure to foetal red cells)
    • If this deadline is missed, administration up to 10 days after sensitising event may be of benefit
  • Dose is dependent on gestation at which sensitising event occurred and size of foeto-maternal haemorrhage
  • Kleihauer test of maternal blood shows the proportion of foetal cells present in the maternal sample (allows calculation of size of foeto-maternal transfusion and amount of extra anti-D required)
  • ALL RhD-negative women who have NOT been previously sensitised should be offered routine antenatal prophylaxis with anti-D either with a single dose regimen at 28 weeks or a two-dose regimen at 28 and 34 weeks
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94
Q

What is the management of Sensitising Events in the RhD-negative Pregnant Woman?

A
  • 1st trimester
    • Foetal blood volume is small so sensitisation is unlikely
    • Anti-D is only indicated following ectopic pregnancy, molar pregnancy, therapeutic TOP and in cases of uterine bleeding which is heavy/repeated or accompanied by abdominal pain
    • 250 IU should be given
  • 12-20 weeks
    • A minimum dose of 250 IU should be administered within 72 hours
    • Kleihauer test should be performed and further anti-D given if indicated
  • 20+ weeks
    • A minimum dose of 500 IU should be given within 72 hours
    • Kleihauer test required to determine added dose
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95
Q

What are signs of foetal anaemia?

A
  • NOTE: not usually obvious unless < 6 g/dL
  • Polyhydramnios
  • Enlarged foetal heart
  • Ascites and pericardial effusions
  • Hyperdynamic foetal circulation
  • Reduced foetal movement
  • Abnormal CTG with reduced variability, eventually a sinusoidal trace
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96
Q

What is the management of Rhesus disease in a sensitised woman?

A
  • Anti-D wont make a difference once the mother has been sensitised
  • Close surveillance is required
  • Rhesus disease gets worse with successive pregnancies
  • It is also important to take into account the rhesus status of the father in subsequent pregnancies (in case the father is different)
  • Antibody levels should be monitored every 2-4 weeks after booking
  • However, titrations of anti-D do not correlate well with the development of HDFN (standard quantification using IU is better)
  • If antibody levels rise, the foetus should be examined for signs of anaemia
  • Middle cerebral artery Doppler scans (peak velocity measurement) correlate with foetal anaemia
  • Treatment includes delivery (if sufficiently mature) or foetal blood transfusion
  • At delivery, blood should always be ready for transfusion
  • ALL babies born to RhD-negative women should have cord blood taken at delivery for blood count, blood group and indirect Coombs’ test
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97
Q

What are the routes of adminstration through transfusions for anti-D?

A
  • Into the umbilical vein at the point of the cord insertion
  • Into the intrahepatic vein
  • Into the peritoneal cavity
  • Into the foetal heart
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98
Q

What are the conditions that require transfused blood?

A
  • RhD-negative
  • Crossmatched with maternal sample
  • Densely packed (so small volumes can be used)
  • White cell depleted
  • Screened for infections (e.g. CMV)
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99
Q

Describe ABO Incompatibility

A
  • Occurs when the mother is group O and the baby is A or B
  • Anti-A and anti-B antibodies are present naturally in the maternal circulation
  • So, ABO incompatibility may occur in a FIRST pregnancy
  • However, most anti-A and anti-B antibodies are IgM so do NOT cross the placenta
  • In addition, A and B antigens are NOT fully developed in the foetus
  • So, ABO incompatibility generally only causes mild haemolytic disease in the newborn
  • NOTE: it is possible to identify the blood group of the foetus by genotyping of cffDNA (this can prevent unnecessary use of anti-D prophylaxis in RhD-negative mothers)
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100
Q

What percentage of live births are multiple pregnancies?

A
  • 3%
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101
Q

Why are the number of multiple pregnancies increasing?

A
  • Increasing use of assisted fertility
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102
Q

What are complications of multiple pregnancies?

A
  • preterm birth, FGR, cerebral palsy and stillbirth
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103
Q

What is the classification of multiple pregnancies?

A
  • Number of foetuses: twins, triplets etc.
  • Number of fertilised eggs: zygosity
  • Number of placentae: chorionicity
  • Number of amniotic cavities: amniocity
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104
Q

Describe dichorionic diamniotic twins

A
  • NOTE: dichorionic diamniotic twins may appear to have one placenta because they anatomically fused together, but they are separate
  • With monozygotic twins, they will be dichorionic diamniotic if the splitting of the zygote occurs soon after fertilisation
  • If the splitting occurs later, they will be monochorionic diamniotic
  • Most monochorionic twins have two amniotic cavities but the dividing membrane is thin, and consists of a single layer of amnion alone
  • If separation occurs even alter (days 8-12), the twins will be monochorionic monoamniotic
  • If it occurs after day 13, the twins will be conjoined
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105
Q

Are women with multiple pregnancies at a higher risk of anaemia than single pregnancies?
What should be done for women with multiple pregnancies?

A
  • Yes
  • FBC should be checked at 20 and 28 weeks
  • Supplementation of iron, folic acid and vitamin B12 should be offered
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106
Q

What physiological changes are exaggerated in multiple pregnancy?

A
  • increased cardiac output, volume expansion, relative haemodilution, diaphragmatic splinting, weight gain and lumbar lordosis
  • ‘minor’ symptoms of pregnancy such as nausea and vomiting may be exaggerated
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107
Q

What are complications of multiple pregnancies?

A
  • Increased morbidity risk
  • About 60% result in spontaneous birth vefore 37 weeks
  • For monochorionic twins, increased chance of preterm birth
  • Increased perinatal mortality in monochorionic twins
  • Infant mortality rate for twins is 5.5 x higher than singletons
  • Stillbirth rate is also higher for twins
  • The death of one foetus in utero, can lead to severe complications for the co-twin (e.g. death, brain damage)
    • It can also lead to onset of labour
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108
Q

How does Multiple pregnancy affect FGR?

A
  • Risk of FGR is higher in each twin compared to singletons
  • This makes certain Doppler studies (e.g. ductus venosus, middle cerebral artery) very difficult
  • Priorities with antenatal management of FGR is to predict the severity of impaired foetal oxygenation and selecting an appropriate time for delivery
  • In dichorionic twins where one foetus is growth restricted, elective preterm delivery may lead to iatrogenic complications to the previously healthy twin
  • In general, delivery should be avoided until after 28-30 weeks
  • The death of one monochorionic twin may result in death or handicap of the co-twin because of acute hypotension due to placental vascular anastomoses between the two circulations
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109
Q

What is twin-to-twin transfusion syndrome?

A
  • Caused by abnormal unbalanced vascular anastomoses
  • Only occurs in monochorionic pregnancies
  • If the vascular connections are unbalanced with more AV connections in one direction than the other, changes in hydrostatic and osmotic forces will occur resulting in the manifestation of TTTS
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110
Q

What are the four types of vascular connections in monochorionic pregnancies?

A
  • Arteriovenous
  • Venoarterial
  • Arterioarterial
  • Venovenous
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111
Q

Which vascular anastamoses are protective against TTTS?

A
  • Arterioarterial
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112
Q

How is TTTS diagnosed?

A
  • Based on ultrasound criteria
  • Single placental mass (i.e. monochorionic)
  • Concordant gender
  • Oligohydramnios with maximum vertical pool < 2 cm in one sac and polyhydramnios in the other sac (> 8 cm)
  • Discordant bladder appearances
  • Haemodynamic and cardiac compromise
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113
Q

How is TTTS graded?

A
  • According to the Quintero staging
  • Stage I: Oligohydroamnios and polyhydroamnios sequence and visualised donor twinbladder. Normal Dopplers in twins
  • Stage II: Oligohydroamnios and polyhydroamnios sequence but non-visualised bladder. Normal dopplers in both twins
  • Stage III: Oligohydroamnios and polyhydroamnios sequence, non-visualised bladder and abnormal Dopplers. There is absent/reverse end-diastolic velocity in the umbilical artery, reverse flow in a-wave of the DV or pulsatile flow in the umbilical veins in either fetus
  • Stage IV: One or both of the fetus show signs of hydrops
  • Stage V: One or both fetuses have died
114
Q

What is twin anaemia polycthymia sequence?

A
  • a rarer chronic forms of TTTS in which a large inter-twin haemoglobin difference occurs
  • NOTE: the oligohydramnios polyhydramnios sequence is NOT seen (unlike in TTTS)
  • Thought to be due to small AV unidirectional anastomoses without accompanying AA anastomoses
  • This leads to gradual development of anaemia in one twin and polycythaemia in the other
  • Polycythaemia can lead to foetal or placental thrombosis
  • Anaemia can lead to hydrops fetalis
  • NOTE: mirror syndrome = combination of foetal hydrops and maternal pre-eclampsia
115
Q

What is recommended to assess growth in multiple pregnancies?

A
  • Serial ultrasound is recommended to assess growth in multiple pregnancies
  • Generally, monochorionic pregnancies will be assessed fortnightly by ultrasound from 16 to at least 24 weeks
116
Q

What is the treatment of twin-to-twin transfusion syndrome?

A
  • Expectant management
  • Amnioreduction
  • Septostomy
  • Selective feticide
  • Fetoscopic laser ablation of vascular anastomoses
    • Considered definitive treatment for severe TTTS (between 16-26 weeks)
    • Involves ablating the AV anastomoses under fetoscopic guidance
  • Above 26 weeks - delivery may be considered
117
Q

What is Monochorionic Monoamniotic Twin Pregnancy?

A
  • Associated with high morbidity and mortality
  • High rate of perinatal morality is due to cord entanglement leading to foetal loss and neurological morbidity
  • They also have increased risk of congenital anomalies (e.g. neural tube defects, abdominal wall malformations)
  • Close surveillance is essential
  • Delivery by Caesarean at 32-34 weeks is generally recommended
  • Usually, patients are hospitalised from 28 weeks gestation and foetal heart auscultation is performed daily (using CTG) to detect signs of cord compression
118
Q

How many appointments should women with uncomplicated dichorionic twin pregnancies be offered?

A
  • At least 8 antenatal appointments
119
Q

How many appointments should women with uncomplicated monochorionic diamniotic twin pregnancies be offered?

A
  • At least 9 antenatal appointments
120
Q

Routine antenatal care for multiple pregnancies involves screening for which conditions?

A
  • Hypertension
  • Gestational diabetes
  • These occur more frequently in MP
121
Q

When should the first trimester scan be done (multiple pregnancy)?

A
  • First trimester scan should be offered when crown-rump length (CRL) measures 45-84 mm
    • This equates to 11 weeks to 13 weeks 6 days
122
Q

What is the purpose of screening (antenatal)?

A
  • To accurately estimate gestational age (based on CRL)
  • To determine chorionicity (by assessing number of placental masses and assessing for lambda or T-sign and membrane thickness)
  • To screen for Down’s syndrome
123
Q

How should amniocentesis and CVS be done in twin pregnancies?

A
  • In dichorionic pregnancies both foetuses must be sampled
124
Q

Describe the anomaly scan and multiple pregnancies

A
  • Higher rates of congenital anomalies (e.g. anencephaly, holoprosencephaly) in MP
  • Only one foetus normally affected by anomalies
  • If only one is affected, it can be managed expectantly or with selective fetocide
  • Non-lethal abnormality may result in handicap, the parents may need to decide whether the potential burden of a handicapped child outweighs the risk of loss of the normal twin from fetocide-related complications
  • If the abnormality is lethal, it may be best to avoid risk to the normal foetus unless the condition itself threatens the survival of the foetus (e.g. anencephaly)
  • Rate of spontaneous dizygotic twinning increases with age
125
Q

Describe growth assessments and multiple pregnancies

A
  • Foetal weight should be calculated from 20 weeks gestation at a maximum of 4 week intervals
  • A growth discrepancy of 25% or more should be considered clinically significant
  • Other indications for tertiary referral include: discordant foetal growth, foetal anomaly, discordant foetal death or TTTS
126
Q

Why must a delivery plan be made for women with multiple pregnancies?

A
  • MP have a high prevalence of preterm delivery
127
Q

What topics to include in the delivery plan of multiple pregnancies?

A
  • Desired mode of delivery
  • Gestation for induction of labour if no spontaneous onset
  • Process of delivery of twin 1 and twin 2
  • Risk of C-section
  • Complications following delivery (e.g. PPH)
  • Desire to breastfeed or not
128
Q

What is the intrapartum management for multiple pregnancies?

A
  • Antenatal education and pre-agreed birth plan
  • Continuous foetal heart monitoring
  • Two neonatal resuscitation trolleys, two obstetricians and two paediatricians
  • Analgesia (ideally an early epidural to allow for internal podalic version of twin 2 if needed)
  • Standard oxytocin solution for augmentation for use in the delivery of the second twin
  • Oxytocin infusion (in anticipated PPH)
  • Portal ultrasound
129
Q

What delivery is recommended for uncomplicated dichorionic diamniotic pregnancy?

A
  • Vaginal delivery provided that the presenting twin is cephalic
  • Complications are less likely if the membranes are not ruptured until the feet of the second twin are held by the operator
130
Q

What happens if the foetus is transverse during delivery?

A
  • External cephalic version can be successful
131
Q

What should happen if external cephalic version is unsuccessful?

A
  • Internal podalic version can be undertaken
    • This is performed by identifying a foetal foot through intact membranes
    • The foot is grasped and pulled gently and continuously into the birth canal
    • The membranes are ruptured as late as possible
132
Q

When is delivery advised for dichorionic twin pregnancy?

A
  • From 37 weeks
133
Q

When is delivery advised for uncomplicated monochorionic twin pregnancy?

A
  • elective delivery from 36 weeks should be offered (it should be performed after a course of antenatal corticosteroids)
134
Q

What does continuing uncomplicated twin pregnancies beyond 38 weeks increase the risk of?

A
  • Intrauterine foetal death
135
Q

What is a support group for multiple pregnancy?

A
  • Twins and Multiple Birth Association (TAMBA)
136
Q

What is preterm labour?

A
  • the onset of labour < 37 weeks gestation
137
Q

What does PPROM stand for?

A
  • preterm premature rupture of membranes
138
Q

What happens to the uterus and cervix during pregnancy?

A
  • During pregnancy the uterus expands to accommodate the growing foetus and remains quiescent
  • At the same time, the cervix remains rigid and closed to retain the developing foetus within the uterus
139
Q

What inhibits myometrial contractility during pregnancy?

A
  • pro-pregnancy factors such as progesterone, relaxin, hCG and pro-relaxation prostaglandins (e.g. prostacyclin)
140
Q

How does onset of labour occur?

A
  • involves synchronisation of myometrial activity through greater expression of gap junctions connecting myometrial cells
141
Q

How is labour diagnosed?

A
  • painful uterine contractions + changes in the structure of the cervix, leading to cervical dilatation and effacement
  • This is part of a gradual process that starts several weeks before delivery
142
Q

What are changes in the cervix during labour due to? (Cellular)

A
  • Breakdown of collagen
  • Changes in proteoglycan concentration
  • Infiltration of leukocytes and macrophages
  • Increase in water content
143
Q

What is increased myometrial activity during labour due to? (ECM)

A
  • Activation of cassette of contraction-associated proteins (CAPs)
  • This converts the myometrium from a quiescent to a contractile state
  • CAPs include gap junction proteins, oxytocin and prostanoid receptors, enzymes for PG synthesis and cell signalling proteins
  • Contractions are a relatively late event in this process, preceded by cervical remodelling and foetal membrane activation
144
Q

What maintain uterine quiescence during pregnancy?

A
  • Progesterone
  • In humans, circulating levels of progesterone remain elevated throughout pregnancy
  • Administration of progesterone receptor antagonist RU486 can induce labour
  • This suggests that the onset of human labour either involves a functional withdrawal of progesterone action or occurs independent of any loss in progesterone activity
  • Current theories for this:
    • Invoking a change in progesterone receptor isoform expression
    • Increase in antagonist PRA isoform
    • Decline in the agonist PRB isoform
    • Repression in PRB activity through activation of NFkB
145
Q

How is Labour an inflammatory process?

A
  • Increased proinflammatory factors (e.g. prostaglandins, cytokines, chemokines)
  • Influx of inflammatory cells into the labouring uterine tissues may result in increased levels of pro-inflammatory cytokines
  • Inflammation is also implicated in infection-driven preterm labour
146
Q

What are the roles of the oxytocin/oxytocin receptor (OTR) system in the pregnant uterus?

A
  • Stimulate contractions
  • Produce prostaglandins
  • There is NO increase in oxytocin production during labour but the sensitivity of the myometrium to oxytocin at term increases
147
Q

What mediates the sensitivity of the myometrium to oxytocin?

A
  • Increased expression of OTR
  • Activation of OTR triggers the release of intracellular calcium, leading to calmodulin-mediated activation of MLCK, which phosphorylates myosin and promotes interaction of myosin with actin and the onset of contractions
148
Q

What do prostaglandins do during labour?

A
  • promote cervical ripening and myometrial contractility
  • Used to induce labour
  • There are both pro-contractile (e.g. PGF2a) and pro-relaxatory (PGI2) prostaglandins
149
Q

What are prostaglandin inhibitors used for? (Labour)

A
  • To inhibit preterm labour (however, they have adverse side-effects such as premature closure of PDA)
150
Q

What is the rate limiting step in PG synthesis?

A
  • PG synthesis enzymes PGHS-2
151
Q

What is the dominant site of PG synthesis?

A
  • Amnion
152
Q

What is the main site of PG action?

A
  • Myometrium
153
Q

What is the main site of PG metabolism?

A
  • Chorion
  • Expresses the enzyme responsible for PG metabolism (15-hydroxyprostaglandin dehydrogenase (PGDH))
  • The expression of PGDH falls with the onset of labour, thus facilitating the transfer of PGs from the amnion to the myometrium
154
Q

What are causes of preterm labour?

A
  • Cervical weakness
  • Infection
  • Uterine Mullerian Anomalies
  • Haemorrhage
  • Stress
  • Multiple pregnancies
155
Q

How does cervical weakness cause preterm labour?

A
  • associated with painless premature cervical dilatation
  • Suggested by a history of painless second trimester pregnancy loss
  • Relationship between cervical length and the risk of preterm delivery
  • Previous history of cervical surgery is a risk factor for cervical weakness
156
Q

How does infection cause preterm labour?

A
  • Infection of the foetal membranes (chorioamnionitis) is a major cause of preterm birth
  • Most of the time the infection ascends from the vagina, however it could be transplacental or introduced through invasive procedures
  • Cervical weakness can predispose to ascending infections
  • 33% of all pregnancies delivered after PPROM are complicated by infection
  • Abnormal vaginal flora (e.g. bacterial vaginosis) is associated with PPROM and PTL
  • Antibiotic treatment of BV does NOT consistently reduce the risk of PTD
157
Q

What is chorioamnionitis associated with in the foetus?

A
  • foetal brain damage due to a foetal inflammatory response
  • Can cause periventricular leukomalacia
  • High levels of amniotic fluid IL-6 is associated with intraventricular haemorrhage and PVL
158
Q

How do Uterine Mullerian Abnormalities cause preterm labour?

A
  • Occur due to abnormal embryologic fusion and canalisation of the Mullerian ducts resulting in an abnormally formed uterine cavity
  • This can range from an arcuate uterus (minimal fundal cavity indentation) to uterine didelphys (complete failure of fusion)
  • These are associated with adverse pregnancy outcomes in up to 25% of women (e.g. PPROM, preterm birth, FGR)
159
Q

How does haemorrhage cause preterm labour?

A
  • Antepartum haemorrhage and placental abruption may lead to spontaneous PTL
  • Acute bleeding —> thrombin release —> myometrial contraction
160
Q

What is placental abruption?

A
  • Separation of the placenta from the wall of the uterus during pregnancy, especially when it occurs prematurely
161
Q

What are risk factors for placental abruption?

A
  • Pre-eclampsia
  • Hypertension
  • Previous abruption
  • Trauma
  • Smoking
  • Cocaine
  • Multiple pregnancy
  • Polyhydramnios
  • Thrombophilia
  • Advanced maternal age
  • PPROM
162
Q

How does stress cause preterm labour?

A
  • Corticotrophin-releasing hormone is implicated
163
Q

How is PTL tested?

A
  • Cervicovaginal fluid level of foetal fibronectin (fFN)
  • glycoprotein found in the cervicovaginal fluid, amniotic fluid, placental tissue and in the interface between the chorion and decidua
  • a glue at the maternal-foetal interface
  • Its presence in the cervicovaginal fluid between 22-36 weeks is a predictor of PTD
  • Negative fFN has a high negative-predictive value (i.e. if it’s negative, you’re almost certainly not in preterm labour)
164
Q

How is preterm labour managed?

A
  • Tocolytics may delay delivery long enough for corticosteroid administration (for neonatal lung function)
  • First choice
    • Calcium channel blocker (e.g. nifedipine)
    • OTR antagonist (e.g. atosiban)
  • Other drugs
    • Beta-sympathomimetics
    • Magnesium Sulphate
    • NSAIDs
    • Corticosteroids
    • Antibiotics
165
Q

How do beta-sympathomimetics manage preterm labour?

A
  • Beta-agonists (ritodrine, salbutamol and terbutaline) are mainly beta-2 agonists
  • Stimulate cAMP production –> myometrial relaxation
  • Delay delivery but do NOT improve neonatal outcome or PTD rates
  • significant maternal side-effects (e.g. pulmonary oedema) `
166
Q

How does magnesium sulphate manage preterm labour?

What does it reduce the risk of in surviving infants?

A
  • Decreases smooth muscle depolarisation by modulating calcium in smooth muscle cells
  • Inhibits uterine contraction
  • American College of Obstetricians believe that it reduces the risk of cerebral palsy in surviving infants
167
Q

How do NSAIDs manage preterm labour?

What risks is Indomethacin associated with?

A
  • Indomethacin is effective
  • Have several adverse foetal effects
  • Inhibition of prostaglandins can lead to premature closure of the ductus arteriosus
    • can lead to persistent pulmonary hypertension
    • This is reversible but requires early identification and discontinuation of treatment
  • Indomethacin is also associated with increased risk of:
    • Necrotising enterocolitis
    • Neonatal renal dysfunction
168
Q

How do CCBs and Oxytocin Receptor Antagonists manage preterm labour?
What is an example of an OTR?

A

Calcium Channel Blockers

  • Relax the contraction of the myometrium
  • They bind to L-type calcium channels and reduce intracellular calcium levels

Oxytocin Receptor Antagonists

  • OTRs are important in the onset and progression of labour
  • Atosiban is a competitive antagonist of oxytocin and vasopressin V1a receptors within the myometrium
  • Atosiban results in a dose-dependent inhibition of uterine contractility and oxytocin-mediated PG release
  • Similar efficacy to beta-agonists but better tolerated
169
Q

How do corticosteroids manage preterm labour?

A
  • Most influence on preterm neonatal outcome
  • Significantly reduces RDS rates
  • Betamethasone and dexamethasone are both recommended
170
Q

How do antibiotics manage preterm labour?

A
  • 10 days of erythromycin is the treatment of choice for PPROM
  • However, antibiotic treatment has no effect in women with intact membranes
171
Q

What is PPROM?

A
  • In 2% of all pregnancies
  • Responsible for 1/3 of preterm deliveries
  • The earlier in pregnancy that PPROM occurs, the shorter the interval to delivery
  • 50% of women deliver within 1 week of PPROM
  • PPROM before 23 weeks may cause pulmonary hypoplasia –> increased risk of neonatal death even if delivery occurs at a later gestational age
  • Diagnosed through clinical history and a pool of liquor on the vagina on speculum examination
  • Management
    • Balancing prematurity risk (if delivery is encouraged) with the risk of maternal/foetal infection (if delivery is delayed)
  • Generally, conservative management is followed in PPROM before 34 weeks unless there is chorioamnionitis
  • Immediate induction of labour is advised in women > 37 weeks gestation
172
Q

What is the conservative management of PPROM?

A
  • Look for signs of chorioamnionitis (including regular recording of maternal temperature, heart rate, CTG and maternal biochemistry)
    • Rising WCC or CRP indicates development of chorioamnionitis
  • Lower genital tract swabs are routinely taken but cultures do NOT correlate well with risk of chorioamnionitis
  • Tocolysis is CONTRAINDICATED due to the increased risk of maternal and foetal infection
173
Q

How can preterm delivery be predicted?

A
  • Past obstetric history
    • Having previous PTD increases risk of PTL
  • Ultrasound measurement of cervical length
    • Direct link between cervical length and risk of PTD
    • Transvaginal ultrasound is better than transabdominal ultrasound
    • Cervical length surveillance with serial measurement of cervical length throughout the 2nd and early 3rd trimester is used to monitor patients at high risk of PTD
174
Q

What are the two main interventions to prevent preterm delivery?

A
  • Progesterone

- Cervical cerclage

175
Q

How does progesterone prevent preterm delivery?

A
  • In women with previous preterm birth, IM hydroxyprogesterone caproate is effective in reducing risk of recurrence
  • It is licensed in the USA for preterm birth prevention in women with previous preterm birth
  • There is NO evidence to show that progesterone can reduce the longer-term adverse effects of preterm birth (e.g. neurodevelopmental disability, respiratory morbidity)
176
Q

How does cervical cerclage?

A
  • May be placed in THREE different circumstances:
    • History indicated cerclage: following multiple midtrimester losses or preterm deliveries
    • Ultrasound indicated cerclage: when the cervix shortens (usually < 25 mm) in women with a history of cervical surgery or previous preterm birth
    • Rescue cerclage: when the cervix is dilating in the absence of contractions
  • Cerclage provides structural support to a weakened cervix
  • This enhances the cervical immunological barrier by improving retention of the mucous plug and preventing ascending infection by maintaining cervical length
  • If transvaginal cerclage fails, transabdominal cerclage may be considered
177
Q

What are the NICE guidelines for prophylactic vaginal progesterone or cervical cerclage?

A
  • Offer progesterone OR cervical cerclage if:
    • History of spontaneous preterm or mid-trimester loss (between 16-34 weeks) of pregnancy
    • AND if transvaginal ultrasound has been carried out between 16-24 weeks of pregnancy and reveals a cervical length < 25 mm
  • Offer progesterone in women with:
    • NO history of preterm birth or mid-trimester loss and transvaginal US scan has been carried out (16-24 weeks) and shows a cervical length < 25 mm
  • Consider cervical cerclage if:
    • A transvaginal US (16-24 weeks) shows cervical length < 25 mm and have either:
      • Had PPROM before
      • OR history of cervical trauma
178
Q

What are the NICE guidelines for diagnosing PPROM?

A
  • If there symptoms suggesting PPROM, offer a speculum examination to look for pooling of amniotic fluid:
    • If pooling is observed: do NOT perform any diagnostic tests but offer care consistent with the woman having PPROM
    • If pooling is NOT observed: consider performing an insulin-like growth factor binding protein-1 test or alpha-microglobulin-1 test of vaginal fluid
      • If these tests are POSITIVE: interpret the results based on the clinical condition and consider offering treatment consistent with the women having PPROM
      • If these tests are NEGATIVE: do NOT offer antibiotic prophylaxis and explain the woman that they are unlikely to have PPROM
  • Do NOT perform diagnostic tests for PPROM if labour becomes established in a woman reporting symptoms suggestive of PPROM
179
Q

What are the NICE guidelines for antibiotic prophylaxis for PPROM?

A
  • Oral erythromycin 250 mg 4/day for 10 days or until labour happens
  • If erythromycin is contra-indicated –> oral penicillin
180
Q

What are the NICE guidelines for identifying infection in women with PPROM?

A
  • Use clinical assessment and tests (CRP, WCC and CTG)

- NOTE: none of these should be used in isolation

181
Q

What are the NICE guidelines for Rescue Cervical Cerclage?

A
  • Do NOT offer to women with any of the following:
    • Signs of infection
    • Active vaginal bleeding
    • Uterine contractions
  • Consider rescue cervical cerclage for women between 16-27 weeks with a dilated cervix and exposed, unruptured foetal membranes
    • Take into account gestational age (benefits are greater for earlier gestations) and extent of cervical dilatation
  • Explain to woman
    • Risks of rescue cerclage
    • That it aims to delay birth, thereby increasing the likelihood of the baby surviving and of reducing serious neonatal morbidity
182
Q

What are the NICE guidelines for diagnosing Preterm Labour with Intact Membranes?

A
  • Clinical assessment should include
    • Clinical history taking
    • Observations
    • Speculum examination (and digital vaginal examination if the extent of cervical dilatation cannot be assessed)
  • If clinical assessment suggests that the woman is in preterm labour and she is < 29+6 weeks pregnant, advise that treatment is necessary
  • If clinical assessment suggests that the woman is in preterm labour and she is > 30 weeks pregnant
    • Consider transvaginal ultrasound measurement of cervical length to determine likelihood of birth within 48 hours
      • If cervical length > 15 mm explain that it is unlikely that she is in preterm labour
      • If cervical length < 15 mm make a diagnosis of preterm labour and treat accordingly
    • Consider foetal fibronectin testing if transvaginal measurement of cervical length is unavailable or unacceptable
      • If negative (concentration < 50 ng/mL) explain that they are unlikely to be in preterm labour
      • If positive (concentration > 50 ng/mL) make a diagnosis of preterm labour and treat accordingly
183
Q

What factors need to be considered when giving tocolysis?

A
  • Is there suspected or diagnosed preterm labour?
  • Other clinical features (e.g. bleeding) which suggest that stopping labour is contraindicated
  • Gestational age at presentation
  • Likely benefit of maternal corticosteroids
  • Availability of neonatal care
  • Maternal preference
184
Q

What are the NICE guidelines for tocolysis?

A
  • Consider Nifedipine if between 24-25+6 weeks, intact membranes and are in suspected or diagnosed preterm labour
  • Nifedipine if between 26-33+6 weeks who have intact membranes and are in suspected or diagnosed preterm labour
  • If nifedipine is contraindicated, offer oxytocin receptor antagonists
  • Do NOT offer beta-mimetics
185
Q

What are the NICE guidelines for maternal corticosteroids?

A
  • For women 23-23+6 weeks in suspected or established preterm labour, having a planned preterm birth or have PPROM, discuss the use of maternal corticosteroids
  • Consider maternal corticosteroids if < 36 weeks with suspected or established preterm labour, having a planned preterm birth or PPROM
186
Q

What are the NICE guidelines for magnesium sulphate for neuroprotection?

A
  • IV magnesium sulphate for women between 24-29+6 weeks who are:
    • In established preterm labour
    • OR having a planned preterm birth within 24 hours
  • Consider IV magnesium sulphate if 30-33+6 weeks who are in preterm labour or having a planned preterm birth within 24 hours
  • Give 4 g IV bolus over 15 mins followed by IV infusion of 1 g/hour until birth or for 24 hours
  • Monitor for clinical signs of magnesium toxicity every 4 hours (pulse, blood pressure, respiratory rate, deep tendon reflexes)
187
Q

What foetal monitoring is considered for preterm labour/delivery?

A
  • CTG is useful
  • Foetal scalp electrode may be considered
  • Foetal blood sampling may be considered
188
Q

What are the NICE guidelines for preterm birth/delivery?

A
  • Discuss benefits of C-section vs vaginal delivery
  • Highlight the difficulties of performing C-section for preterm birth, particularly the increased likelihood of vertical incision and its implications for future pregnancies
  • Explain that there are NO known benefits or harms for the baby from C-section (but evidence is limited)
  • Consider C-section if in breech position and preterm
189
Q

Describe pre-pregnancy counselling for women with renal disease

A
  • Women should be made aware of the risks to the foetus and the impact on long-term renal function before conception
  • Topics to discuss
    • Safe contraception
    • Fertility issues if indicated
    • Genetic counselling if inherited disorder
    • Risks to mother and foetus during pregnancy
    • Avoid known teratogens and contraindicated drugs
    • Treatment of blood pressure and adjustment of antihypertensives
    • Low-dose aspirin
    • Need for anticoagulation once pregnant in women with significant proteinuria
      • Need for strict surveillance
      • Likelihood of prolonged admission and early delivery
      • Possibility of accelerated decline in maternal renal function
      • Need for postpartum follow-up
190
Q

What is the effect of pregnancy on CKD?

A
  • Women with CKD stages 1-2 will usually be fine
  • Women with CKD stages 3-5 = at risk of complications during pregnancy and decline in renal function
  • Diagnosis of pre-eclampsia can be difficult because of pre-existing hypertension/proteinuria
191
Q

What is the effect of CKD on pregnancy outcome?

A
  • Increased risk of:
    • Preterm delivery
    • Delivery by C-section
    • FGR
192
Q

How do you monitor patients with CKD?

A
  • Blood pressure
  • Renal function
    • Creatinine
  • Urine
    • Infection
    • Proteinuria
  • FBC
    • Haemoglobin
    • Ferritin
  • Renal ultrasound
  • Foetal ultrasound
    • Anatomy
    • Uterine artery Doppler 20-24 weeks
    • Growth
193
Q

What are the complications of dialysis in pregnancy?

A
  • Preterm delivery
  • Polyhydramnios
  • Pre-eclampsia
  • Caesarean delivery
  • Dialysis should be adjusted to allow for physiological changes in pregnancy (plasma volume, fluid retention, electrolytes)
  • Haemodialysis is more effective
194
Q

How do renal transplants affect pregnancy?

A
  • Conception is rare in end-stage kidney disease but fertility returns rapidly after renal transplantation
  • Pregnancy is generally safe after the 2nd post-transplantation year
  • ALL pregnancies in transplant recipients are high risk
  • Vaginal delivery is considered safe
  • Tacrolimus, azathioprine, ciclosporin and prednisolone are considered SAFE in pregnancy and breastfeeding
  • Screening for GDM is necessary with prednisolone and tacrolimus
  • Mycophenolate and sirolimus should be avoided in transplant recipients considering pregnancy and alternative regimes should be considered
195
Q

What are the complications of pregnancy in transplant recipients?

A
  • Preterm delivery
  • Pre-eclampsia
  • UTI
196
Q

Describe pre-pregnancy counselling for diabetes mellitus

A
  • Counsel to achieve the best possible glycaemic control before pregnancy
  • Educate about the implications of diabetes in pregnancy
  • Poor glycaemic control is associated with increased risk of congenital anomalies (particularly NTDs and cardiac anomalies)
  • The most critical period for the embryo is the first 42 days, during organogenesis
  • HbA1c in early pregnancy correlated with the risk of early foetal loss
  • Adequate contraception should be encouraged until glucose control is good
  • Target for pre-pregnancy = pre-meal glucose levels of 4-7 mmol/L
  • Women with complications of diabetes (e.g. retinopathy) will benefit from an MDT approach
  • Diabetic nephropathy is associated with significantly increased risk of complications arising in pregnancy warranting preterm delivery
197
Q

What are the maternal and foetal complications in diabetes mellitus?

A
  • Congenital abnormality is 2-4 times more likely in diabetic pregnancies
  • Foetal macrosomia (and consequently traumatic birth, shoulder dystocia)
  • Accelerated growth patterns in the late second and third trimesters
  • Stillbirth
  • Increased risk of pre-eclampsia
  • Progression of diabetic retinopathy
  • Infection
  • Severe hyper- or hypoglycaemia and DKA
  • IMPORTANT: all women with diabetes should be offered low-dose (75 mg) aspirin from 12 weeks gestation until delivery
198
Q

What is the management of diabetes mellitus in pregnancy?

A
  • MDT approach involving:
    • Diabetic specialist midwives and nurses
    • Dietician
    • Obstetrician
    • Physician
  • Monitor blood glucose 7 times per day (before and 1 hour after meals)
  • Pre-meal target < 5.3 mmol/L
  • 1-hour postprandial target < 7.8 mmol/L
  • Support for diet, oral hypoglycaemics and insulin adjustments
  • IMPORTANT: hypoglycaemia is more common in pregnancy and is very dangerous
  • Insulin resistance INCREASES throughout pregnancy, so women with DM need to increase metformin or insulin during the second half of pregnancy
  • Pregnancy plan should include
    • Renal and retinal screening
    • Foetal surveillance
    • Plan for delivery
  • Women with DM to have a foetal anomaly scan at 19-20 weeks with an assessment of cardiac outflow tracts
  • Serial growth scans to assess foetal growth and diagnose macrosomia and polyhydramnios
  • IMPORTANT: if antenatal corticosteroids are needed, additional insulin therapy is required to maintain normoglycaemia (often requires admission)
  • If the pregnancy has gone well, the aim should be to achieve vaginal delivery between 38-39 weeks
  • However, presence of complications means that the C-section rate amongst diabetic women is quite high (around 50%)
  • For women with T1DM or T2DM requiring insulin, a sliding scale or insulin and glucose should be commenced in labour
  • Maternal glucose levels should be maintained at 4-7 mmol/L
  • Insulin requirements return to pre-pregnancy levels following delivery and insulin doses should be adjusted accordingly
199
Q

What are the effects of pregnancy on diabetes?

A
  • Nausea and vomiting (particularly early on)
  • Greater importance of tight glucose control
  • Increase in insulin dose requirements in second half of pregnancy
  • Increased risk of severe hypoglycaemia
  • Risk of deterioration of pre-existing retinopathy
  • Risk of deterioration of established nephropathy
200
Q

What are the effects of diabetes on pregnancy?

A
  • Increased risk of miscarriage
  • Risk of congenital malformation
  • Risk of macrosomia
  • Increased risk of pre-eclampsia
  • Increased risk of stillbirth
  • Increased risk of infection
  • Increased operative delivery rate
201
Q

Describe gestational diabetes

A
  • Complicates 10-15% of pregnancies
  • Women with GDM are at increased risk of T2DM in later life
  • Education about diet and lifestyle important
  • Screening is targeted at HIGH RISK groups (e.g. ethnicity, family history, maternal obesity)
  • IMPORTANT: different diagnostic criteria are used in different hospitals
202
Q

What are the NICE recommendations for diagnosing gestational diabetes?

A
  • Fasting blood glucose > 5.6 mmol/L

- 2-hour OGTT (75 g glucose) > 7.8 mmol/L

203
Q

What are the WHO recommendations for diagnosing gestational diabetes?

A
  • Fasting blood glucose > 5.1 mmol/L
  • 1-hour OGTT > 10 mmol/L
  • 2-hour OGTT > 8.5 mmol/L
204
Q

What is the management of gestational diabetes?

A
  • Principles are the same as diabetes mellitus
  • Encourage women to maintain blood glucose levels:
    • Pre-meal < 5.3 mmol/L
    • Postprandial (1 hour) < 7.8 mmol/L
  • Metformin and/or insulin if unable to achieve levels with diet/lifestyle
  • IMPORTANT: in women with GDM, a diagnosis of T2DM should be excluded after pregnancy
    • Screening with fasting blood glucose or HbA1c should be offered at 6-13 weeks after childbirth
205
Q

What are the factors associated with poor pregnancy outcome in diabetes?

A
  • Maternal social deprivation
  • No folic acid intake pre-pregnancy
  • Suboptimal approach of the woman to managing her diabetes
  • Suboptimal preconception care
  • Suboptimal glycaemic control at any stage
  • Suboptimal maternity care during pregnancy
  • Suboptimal foetal surveillance of big babies
206
Q

What are thyroid related physiological changes in pregnancy?

A
  • Plasma volume expansion
  • Increased thyroid binding globulin
  • Relative iodine deficiency
207
Q

What happens to the thryoid in the first trimester?

A
  • Fall in TSH and rise in free T4 is expected

- Free T4 will then fall with advancing gestation

208
Q

What is the most common cause of hypothyroidism?
How should hypothyroidism be managed in pregnancy?
What is suboptimal management associated with?

A
  • Hashimoto’s thyroiditis is the most common cause of hypothyroidism in the developed world
  • Women should continue thyroid replacement therapy throughout pregnancy and should aim for biochemical euthyroidism (TSH < 4 mmol/L)
  • TFTs performed each trimester, or more often if dose adjustments are required
  • Corrected hypothyroidism has no influence on pregnancy outcome or complications
  • Suboptimal replacement is associated with developmental delay and pregnancy loss
209
Q

How should hyperthyroidism be treated in pregnancy?
Why is radioactive iodine contraindicated in pregnancy?
What is the medication for hyperthyroidism?

A
  • Should be treated medically in pregnancy
  • Radioactive iodine is CONTRAINDICATED because it obliterates the foetal thyroid
  • Carbimazole or propylthiouracil at the lowest acceptable dose
    • High doses may cross the placenta causing foetal hypothyroidism
    • WARNING: both drugs can cause agranulocytosis so regularly check maternal WCC
  • Thyroid function should be closely monitored and many women can reduce their dose (1/3 are able to stop treatment)
  • Doses readjusted postpartum to prevent relapse
  • TSH-receptor stimulating antibodies can cross the placenta, so babies born to women with positive antibody titres should be reviewed by the neonatology team
210
Q

What are the risks of uncontrolled thyrotoxicosis in pregnancy?

A
  • Increased risk of miscarriage
  • Preterm delivery
  • FGR
211
Q

What is thyroid storm and what are its features?

A
  • LIFE-THREATENING
  • Usually caused by under-treatment or infection
  • Features
    • Excessive sweating
    • Pyrexia
    • Tachycardia
    • Atrial fibrillation
    • Hypertension
    • Hyperglycaemia
    • Vomiting
    • Agitation
    • Cardiac failure
212
Q

What is the management of a thyroid storm?

A
  • Propylthiouracil
  • High-dose corticosteroids
  • Beta-blockers (to block peripheral effects)
  • Rehydration
213
Q

How is hyperparathyroidism managed in pregnancy?

A
  • Parathyroidectomy for severe cases

- Mild hyperparathyroidism= adequate hydration and low calcium diet

214
Q

What are the risks of hyperparathyroidism in pregnancy?

A
  • Increased rates of miscarriage
  • Intrauterine death
  • Preterm labour
  • Neonatal tetany
215
Q

What are the risks of hypoparathyroidism in pregnancy?

A
  • Increased risk of second trimester miscarriage
  • Foetal hypocalcaemia
  • Neonatal rickets
216
Q

What is the management of hypoparathyroidism in pregnancy?

A
  • Vitamin D
  • Oral calcium supplements
  • Regular monitoring of calcium and albumin
217
Q

What is hyperprolactinaemia caused by?
What does it cause?
How is it treated?

A
  • Hyperprolactinaemia is usually caused by a benign pituitary microadenoma
  • NOTE: it is an important cause of infertility
  • 80% of cases are treated with a dopamine agonist (bromocriptine or cabergoline) which causes tumours to reduce in size
  • Larger tumours may require surgery or radiotherapy (should be done before pregnancy)
  • The pituitary gland enlarges by 50% during pregnancy
  • Microadenomas do NOT tend to cause issues during pregnancy
  • Dopamine agonists are usually stopped during pregnancy
  • Visual fields and relevant symptoms (e.g. frontal headache) are monitored
  • If there is evidence of tumour growth, dopamine agonist should be recommenced
218
Q

How does Cushing’s syndrome affect pregnancy?

A
  • Rare because most affected women are infertile
  • In pregnancy, adrenal causes are more common
  • Diagnosis can be difficult because a lot of symptoms are normal in pregnancy (e.g. abdominal striae, weight gain, weakness, glucose intolerance)
219
Q

What are the risks of Cushing’s syndrome in pregnancy?

A
  • Pre-eclampsia
  • Preterm delivery
  • Stillbirth
220
Q

How does Conn’s syndrome affect pregnancy?
What are its features?
How is it diagnosed?

A
  • One of the more common causes of secondary hypertension
  • Characterised by hypertension and hypokalaemia
  • Diagnosed by detecting high aldosterone and low renin
  • Enlargement of adrenals can be seen on CT or US
221
Q

What are the symptoms of Addison’s disease?

A
  • Exhaustion
  • Nausea
  • Hypotension
  • Hypoglycaemia
  • Weight loss
222
Q

Why is diagnosis of Addison’s disease difficult in pregnancy?

A
  • Diagnosis can be difficult because the cortisol levels may be erroneously in the normal range because of an increase in cortisol-binding globulin during pregnancy
223
Q

How should pregnant Addison’s patients be managed?

A
  • If the patient presents in an Addisonian crisis, they should be treated with fluid rehydration and corticosteroids
  • Replacement steroids should continue throughout pregnancy with increased doses at times of stress (e.g. delivery)
224
Q

How does Phaeochromocytoma in pregnancy present and how is it diagnosed?

A
  • May present as a hypertensive crisis (may appear similar to pre-eclampsia)
  • Diagnosed by measurement of catecholamines in 24-hr urine collection and adrenal imaging
225
Q

How is phaeochromocytomas in pregnancy managed?

A
  • Alpha and beta blockade (e.g. prazosin, phenoxybenzamine)
  • Surgical removal is the only cure
  • C-section is the preferred mode of delivery (prevents sudden increases in catecholamines associated with vaginal delivery)
  • Maternal and perinatal mortality is increased if NOT diagnosed before pregnancy
226
Q

What is the antenatal management of heart disease?

A
  • Joint obstetric/cardiac management
  • Assess level of heart failure (NYHA classification)
  • Routine physical examination should include pulse rate, blood pressure, jugular venous pressure, heart sounds, ankle and sacral oedema and the presence of basal crepitations
  • Most women will remain well throughout pregnancy
  • An echocardiogram at booking and at 28 weeks
  • Anticoagulation is essential in patients with congenital heart disease who have pulmonary hypertension or artificial valves and those at risk of AF
  • WARNING: warfarin is teratogenic if used in the first trimester
    • LMWH is used as an alternative (especially in 1st and 3rd trimester)
227
Q

What are high risk cardiac conditions in pregnancy?

A
  • Systemic ventricular dysfunction
  • Pulmonary hypertension
  • Cyanotic congenital heart disease
  • Aortic pathology (e.g. Marfan syndrome)
  • Ischaemic heart disease
  • Left heart obstructive lesions (e.g. aortic/mitral stenosis)
  • Prosthetic heart valves
  • Previous peripartum cardiomyopathy
228
Q

What are foetal risks of maternal cardiac disease?

A
  • Recurrence (congenital heart disease)
  • Maternal cyanosis (foetal hypoxia)
  • Iatrogenic prematurity
  • FGR
  • Effects of maternal drugs (teratogenesis, growth restriction, foetal loss)
229
Q

What is the management of labour and delivery in heart disease?

A
  • In most cases, try wait for spontaneous labour
  • Induction maybe in very high-risk women so delivery occurs at a predictable time with all the personnel present
  • Epidural anaesthesia recommended (reduces pain-related stress)
    • NOTE: there is, however, risk of maternal hypotension
  • Prophylactic antibiotics given to woman with a structural heart defect to reduce the risk of bacterial endocarditis
  • If labour progresses normally, the second stage may be kept short with an elective forceps or ventouse delivery
  • This reduces maternal effort and the requirement for increased cardiac output
  • C-section should be reserved for cases where the maternal condition is too unstable to tolerate the demands of labour
  • Postpartum haemorrhage may lead to cardiovascular instability
  • Ergometrine may be dangerous (causes vasoconstriction, hypertension and heart failure) so active management of the third stage is with syntocinon ALONE
    • NOTE: syntocinon is a vasodilator so should be introduced slowly
Summary
- Avoid induction of labour if possible  
- Use prophylactic antibiotics  
- Ensure fluid balance  
- Avoid supine position  
- Discuss regional/epidural anaesthesia with senior anaesthetist 
- Keep the second stage short  
Use syntocinon judiciously
230
Q

What is the treatment of heart failure in pregnancy?

A
  • The principles of treatment are the same as in non-pregnant people
  • Clinical examination and echocardiography to confirm ventricular dysfunction is important
  • Typical management of heart failure
    • Sit up
    • Oxygen
    • Diamorphine
    • Furosemide
    • GTN
  • Arrhythmias require urgent correction and drug therapy
  • Assess foetal wellbeing (US and CTG)
  • Consider premature delivery if foetal compromise
231
Q

(What is the primary cause of MI in the postpartum period?
Why should PCI be considered carefully?
What does thrombolysis increase the risk?)

A
  • Coronary artery dissection is the primary cause of MI in the postpartum period
  • PCI increases risk of radiation to the foetus)
  • Thrombolysis may increase haemorrhage risk
232
Q

Describe mitral and aortic stenosis in pregnancy

A
  • Obstruction of the left heart leads to an inability to increase cardiac output to meet the demands of pregnancy
  • 40% of those with mitral stenosis (usually due to rheumatic fever) will experience worsening symptoms during pregnancy
  • Treatment aims to reduce heart rate (through bed rest, oxygen, beta-blockade and diuretic therapy)
  • Balloon mitral valvotomy is the treatment of choice after delivery
  • The risk of maternal morbidity and mortality is correlated to the severity of the disease
233
Q

Describe pulmonary hypertension in pregnancy

A
  • Pulmonary hypertension has a poor survival

- Pregnancy is associated with high risk of maternal death

234
Q

How does bacterial and viral pneumonia occur in pregnancy?

A
  • Viral pneumonia follows a more complicated course in pregnancy and can lead to quicker decompensation
  • Bacterial pneumonias are managed in the same way as in non-pregnant women
235
Q

What are warning signs of pnuemonia?

A
  • Respiratory rate > 30/minute
  • Hypoxaemia: pO2 < 7.9 kPa on room air
  • Acidosis: pH < 7.3
  • Hypotension
  • DIC
  • Elevated blood urea
  • Evidence of multiple organ failure
236
Q

Describe asthma and pregnancy

A
  • Asthma severity and suboptimal control are associated with adverse outcomes
  • Labour and delivery are NOT usually affected by asthma
  • Regular medications should be continued throughout labour (ALL the asthma drugs are safe to use)
  • Bronchoconstrictors (e.g. ergometrine or prostaglandin F2a) should be avoided in women with severe asthma
  • Regional anaesthesia is favoured over general anaesthesia
  • Postpartum, there is NO increased risk of exacerbations
237
Q

How is asthma managed in pregnancy?

A
  • Pregnancy is a time to improve asthma care
  • Encourage smoking cessation
  • Ensure patient education regarding condition and adequate use of medications
  • Ensure optimal control and response to therapy throughout pregnancy
  • Manage exacerbations aggressively and avoid delays in treatment
  • Manage acute attacks as in non-pregnant individual
  • Offer an MDT approach
238
Q

Describe cystic fibrosis and pregnancy

A
  • High rate of prematurity
  • 70-90% live births
  • The prognosis for the mother depends on the severity of the CF
  • Most women will have daily physiotherapy and prolonged antibiotic therapy
  • Close attention should be paid to maternal nutritional status and weight gain during pregnancy, with screening for GDM
  • CF is associated with FGR so foetal ultrasound scans should be regularly performed
  • Check the CF carrier status of the partner
  • Ideally, a vaginal delivery should be the aim
239
Q

Does pregnancy affect sarcoidosis?

A
  • Pregnancy does NOT affect the long-term natural history of sarcoidosis
240
Q

How does epilepsy affect pregnancy?

A
  • No consistent effect of pregnancy on epilepsy
  • 10 fold increase in mortality amongst pregnancy women with epilepsy
  • Seizures should be controlled with the minimum possible dose of the optimal anticonvulsant drug
  • Epilepsy is associated with an increased risk of congenital abnormality caused by anticonvulsant medication (2-3 fold increase)
  • Use of several AEDs further increases risk
241
Q

What is the pre-pregnancy counselling of epilepsy?

A
  • Alter medication according to seizure frequency
  • Reduce to monotherapy where possible
  • Stress importance of compliance with medication
  • Preconceptional folic acid 5 mg
  • Explain risk of congenital malformation
  • Explain risk from recurrent seizures
242
Q

What are the main abnormalities associated with AEDs?

A
  • Neural tube defects
  • Facial clefts
  • Cardiac defects
  • (developmental delay, nail hypoplasia, growth restriction and midface abnormalities)
  • NOTE: valproate should be avoided unless unresponsive to other AEDs
  • Many of these can be detected during an anomaly scan
243
Q

What can stopping anticonvulsant therapy during pregnancy result in?

A
  • Increased frequency of epileptic seizures resulting in both maternal and foetal hypoxia
244
Q

What is the management of pregnant epilepetic patients ?

A
  • Switched to monotherapy before pregnancy
  • 5 mg folic acid to reduce risk of NTDs
  • Delivery mode and timing is unaltered by epilepsy unless there is accelerated seizure frequency
  • Breastfeeding should be encouraged
245
Q

What are causes of seizures in pregnancy?

A
  • Epilepsy
  • Eclampsia
  • Encephalitis or meningitis
  • SOL
  • Cerebrovascular accident
  • Cerebral malaria or toxoplasmosis
  • TTP
  • Drug and alcohol withdrawal
  • Toxic overdose
  • Metabolic abnormalities (e.g. hypoglycaemia)
246
Q

Describe multiple sclerosis in pregnancy

A
  • Pregnant women with MS have no higher risk of complications
  • Women will have a lower relapse rate during pregnancy
  • They will, however, have a higher relapse rate in the 3 months postpartum
  • Delivery is NOT more complicated in MS patients
247
Q

Describe migraines in pregnancy

A
  • Usually improves in pregnancy
  • 20% of pregnant women experience migraines
  • Management should include analgesics and antiemetics
  • Low-dose aspirin and beta-blockers may be used to prevent attacks
248
Q

Describe Bell’s palsy in pregnancy

A
  • Incidence increases 10 fold in the third trimester
  • Complete recovery is expected if it occurs within 2 weeks of delivery
  • Corticosteroids and antivirals may be used in pregnancy
249
Q

How does pregnancy affect sickle cell disease?

What medication is recommended for pregnancy?

A
  • Pregnancy is associated with increased risk of sickle cell crises
  • High-dose folate (5 mg) is recommended preconception
  • Low-dose aspirin (75 mg) daily from early pregnancy to delivery
  • HbSC is associated with mild anaemia but can cause very severe crises that occur more often in pregnancy
250
Q

What are sickle cell crises precipitated by?

A
  • Hypoxia
  • Stress
  • Infection
  • Haemorrhage
251
Q

What are sickle cell mothers at increased risk of?

A
  • Miscarriage
  • Pre-eclampsia and eclampsia
  • FGR
  • Premature labour
  • Thromboembolic disease
252
Q

What is the management of sickle cell crisis in pregnancy?

A
  • Prompt treatment
  • Adequate hydration
  • Oxygen
  • Analgesia
  • Screen for infection (urinary, respiratory)
  • Antibiotics
  • Blood transfusion
  • Exchange transfusion
  • Prophylaxis against thrombosis (heparin)
  • Foetal monitoring
253
Q

Describe thalassaemia in pregnancy

A
  • MOST COMMON genetic blood disorder
  • If alpha or beta thalassemia minor, the patients will be mildly anaemic but there are no other issues
  • Iron and folate supplements should be given
  • The partner should be screened
254
Q

What is thrombocytopaenia defined as in pregnancy?

How is gestational thrombocytopaenia diagnosed?

A
  • Platelet count < 150 x 109/L
  • Gestational thrombocytopaenia occurs in 7-8% of pregnancies
  • Bleeding is rarely a complication unless platelet count drops < 50 x 109/L
  • Autoimmune and other causes of thrombocytopaenia should be excluded before arriving at a diagnosis of gestational thrombocytopaenia
  • NO intervention is required other than monitoring platelet count
  • Spontaneous resolution occurs after delivery
255
Q

What are the causes of thrombocytopaenia in pregnancy?

A
  • Idiopathic
    • Increased consumption or destruction
    • Autoimmune
    • Antiphospholipid syndrome
    • Pre-eclampsia
    • HELLP syndrome
    • DIC
    • TTP
    • Hypersplenism
  • Decreased production
    • Sepsis
    • HIV
    • Malignant bone marrow infiltration
256
Q

Describe autoimmune thrombocytopaenia in pregnancy

A
  • Autoantibodies destroy platelets

- Maternal haemorrhage may occur if platelet count < 50 x 109/L

257
Q

What is the management of autoimmune thrombocytopaenia in pregnancy?

A
  • Serial monitoring of platelet count
  • Treatment should be considered if count falls < 50 x 109/L approaching 37 weeks
  • Corticosteroids suppress platelet autoantibodies (but high doses can lead to weight gain, hypertension and diabetes)
  • IVIG increases platelet count more quickly
  • Vaginal delivery should be facilitated and regional anaesthesia should be avoided 80 x 109/L
  • A cord blood sample should be collected for platelet count
258
Q

What are different bleeding disorders during pregnancy and delivery?

A
  • Inherited
    • Vascular abnormalities
    • Platelet disorders
    • Coagulation disorders
  • Acquired
    • Thrombocytopaenia
    • DIC
    • Acquired coagulation disorders
    • Marrow disorders
259
Q

What are inherited coagulation disorders in pregnancy?

A
  • Carriers of haemophilia A and B usually have clotting factor activity that is 50% of normal
  • Factor 8C and vWF antigen activity increase during pregnancy (may buffer the effect of mild disease)
  • In haemophilia carriers, tests to confirm foetal sex should be offered (either ultrasound or cffDNA)
  • Women with bleeding disorders are at significant risk of postpartum haemorrhage
  • Planning for delivery is guided by third trimester clotting factor levels (taking into account the bleeding tendency)
  • Factor concentrate, tranexamic acid and desmopressin may be used in labour and delivery for women deemed to be at significant risk
  • NOTE: DDAVP increases levels of factor 8 and vWF
  • Invasive foetal monitoring, ventouse and rotational forceps should be avoided if there is a risk that the foetus may be affected by the disease
260
Q

Describe Peptic Ulcer Disease in pregnancy?

A
  • Less common in pregnancy and pre-existing ulceration tends to improve
  • Probably due to altered oestrogen levels and improved diet
  • Antacids and antiulcer medication is safe
  • Pregnancy is NOT a contraindication for endoscopy
261
Q

What is untreated coeliac disease associated with in pregnancy?

A
  • Spontaneous miscarriage
  • FGR
  • Gluten-free diet enables healthy pregnancy outcome
262
Q

Describe IBD and pregnancy

A
  • Women with IBD have lower fertility rates
  • Disease flares during pregnancy is more likely if the disease is active at conception
  • Uncontrolled disease activity at conception is associated with an adverse pregnancy outcome
  • Flares in the first trimester and postpartum are most common
  • High-dose (5 mg) folic acid is recommended
  • Other vitamin supplementation may be required
263
Q

What are the risks of IBD in pregnancy?

A
  • Increased rate of delivery by C-section
    • NOTE: it is indicated if there is active perianal disease
  • Preterm labour
  • SGA
264
Q

Which IBD medication is contraindicated in pregnancy?

How is IBD managed in pregnancy?

A
  • Methotrexate CONTRAINDICATED in pregnancy
  • Other medications (e.g. 5-ASA, azathioprine, ciclosporin, infliximab and corticosteroids) are low risk
  • A relapse of IBD during pregnancy should be treated with STEROIDS (tablets, IM injection or enema)
265
Q

How are pancreatitis and pregnancy linked?

A
  • Uncommon
  • Usually caused by gallstones or alcohol
  • Management is supportive
266
Q

Describe viral hepatitis and pregnancy

A
  • MOST COMMON cause of jaundice in pregnancy worldwide

- Acute viral hepatitis in the first trimester is associated with increased risk of spontaneous miscarriage

267
Q

Describe Hepatitis E and pregnancy
Which pregnancy factors are more commonly associated with Hep E?
What complications is Hep E associated with?

A
  • Hepatitis E infection is more likely to lead to fulminant hepatic failure in pregnancy
  • Most common in primigravida and in the third trimester
  • It is also associated with
    • Preterm delivery
    • FGR
    • Stillbirth
268
Q

What virus can also cause hepatitis in pregnancy?

A
  • Herpes simplex
269
Q

Describe Hep B & C in pregnancy

A
  • Hepatitis B is associated with a 20-30% risk of foetal transmission
  • Hepatitis C is associated with:
    • Preterm rupture of membranes
    • GDM
    • LBW
    • Neonatal unit admission
270
Q

How does autoimmune hepatitis affect pregnancy?

A
  • Characterised by progressive hepatic parenchymal destruction (eventually leading to cirrhosis)
  • Diagnosed on liver biopsy and is associated with ASMA and ANA
  • High foetal loss rate when autoimmune hepatitis is active during pregnancy
  • Immunosuppressive therapy should be continued during pregnancy according to disease activity
271
Q

Describe gallstones in pregnancy

A
  • Increased oestrogen levels leads to increased cholesterol secretion and supersaturation of bile
  • Increased progesterone levels leads to decreased small intestinal motility
  • Conservative management is recommended initially (especially in 1st and 3rd trimester)
  • Medical management involves:
    • IV fluids
    • Correction of electrolytes
    • Bowel rest
    • Pain management
    • Broad-spectrum antibiotics
  • Relapse rates are high during pregnancy and may require surgery (ideally in 2nd trimester)
272
Q

How does pregnancy affect SLE?
What are the risks of SLE and pregnancy?
Which SLE women have the highest risk of adverse outcomes?

A
  • Pregnancy increases the risk of flares
  • They are most common in the late 2nd and 3rd trimester
  • Risks
    • Miscarriage
    • Foetal death
    • Pre-eclampsia
    • Preterm delivery
    • FGR
  • Women with lupus nephritis are at highest risk of adverse outcomes
273
Q

What is antiphospholipid syndrome?

What are its clinical features?

A
  • Association of anticardiolipin antibodies and/or lupus anticoagulant with the typical clinical features of:
    • Arterial or venous thrombosis
    • Foetal loss after 10 weeks’ gestation
    • 3+ miscarriages at < 10 weeks gestation or delivery < 34 weeks due to FGR or pre-eclampsia
  • Furthermore, positive antibody titres must be present on 2 occasions, 3 months apart
  • Antiphospholipid syndrome may be primary or found in SLE
274
Q

How should antiphospholipid syndrome be managed in pregnancy?

A
  • Intensive monitoring
  • Low-dose aspirin to start by 12 weeks gestation
  • Baseline renal studies including a 24-hour urine collection for protein
  • Monitor BP (because of risk of pre-eclampsia)
  • Serial ultrasonography should be performed to assess foetal growth, umbilical artery Doppler and liquor volume
  • If treatment is required, steroids, azathioprine, sulfasalazine and hydroxychloroquine can be given safely
  • NSAIDs can be given until week 32
  • Some mother with SLE will have anti-Ro/La antibodies which cross the placenta and can cause neonatal lupus (usually manifests as cutaneous lesions) and congenital heart block (high perinatal mortality)
275
Q

How is rheumatoid arthritis affected in pregnancy?

A
  • Most women experience improvement during pregnancy
  • 90% will flare up postpartum
  • There are no adverse effects in pregnancy
  • Corticosteroids are preferred to NSAIDs
276
Q

What physiological changes occur in the skin during pregnancy?

A
  • Increased pigmentation
  • Spider naevi
  • Pruritus without rash
277
Q

How does pregnancy affect pre-existing skin disease?

A
  • Atopic eczema and acne can worsen in pregnancy
278
Q

What is Pemphigoid Gestationis?

How is it managed?

A
  • Rare pruritic autoimmune bullous disorder
  • Lesions begin on the abdomen progressing to widespread clustered blisters sparing the face
  • Managed using topical and oral steroids
279
Q

What is polymorphic eruption of pregnancy?

A
  • Self-limiting pruritic inflammatory disorder usually presenting in 3rd trimester
  • Often begins on the lower abdomen involving pregnancy striae and extends to the thighs, buttocks, legs and arms
  • Tends to spare the umbilicus, face, hands and feet
  • The lesions usually become confluent and widespread
  • No tendency to recur
  • No impact on pregnancy
280
Q

What is prurigo of pregnancy?

A
  • Common
  • Excoriated papules on extensor limbs, abdomen and shoulders
  • More common in women with a history of atopy
  • Usually starts around 25-30 weeks
  • Resolves after delivery
  • Treated with topical steroids and emollients
281
Q

What is pruritic folliculitis of Pregnancy?

A
  • Pruritic follicular eruption with papules and pustules mainly affecting the trunk
  • Looks similar to acne
  • Usually starts in 2nd and 3rd trimester
  • Resolves within weeks of delivery