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1
Q

What are the RFs for high risk/abnormal pregnancies?

A
  • extremities of age
  • pre pregnancy weight < 45kg or obesity
  • height <5ft
  • incompetent cervix
  • uterine malformations
  • small pelvis
  • single woman
  • drugs
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2
Q

What are the pre-existing conditions that make pregnancies high risk?

A
  • HT
  • seizures
  • thyroid disease
  • auto-immune conditions
  • infections
  • kidney disease
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3
Q

What are the conditions in pregnancy that complicate it?

A
  • pre eclampsia
  • kidney infection
  • infections
  • Rh incompatibility
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4
Q

What investigations should be done in high risk pregnancies?

A
  • Clinical assessment
  • Urine: protein: creatinine, nitrates, leucocytes and MSU
  • Bloods: FBC, U&Es, lFTs, OGTT
  • USS
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5
Q

What managements are there for high risk pregnancies?

A
  • Surveillance for high risk patients
  • Offer high dose of folate (5mg)
  • Offer low dose aspirin as prophylaxis
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6
Q

Define oligohydramnios

A

Decreased volume of amniotic fluid, below 5th centile, or deepest pool<2cm.

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7
Q

What are the RFs for oligohydramnios?

A
  • ROM
  • Placental insufficiency
  • Foetal urinary tract malformation
  • Chr abnormality
  • Post-term pregnancy
  • IUGR
  • Pre-eclampsia
  • Medication
  • Multiple pregnancy
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8
Q

How would oligohydramnios present?

A

history of fluid leak PV

commonly asymptomatic

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9
Q

What investigations should be done to assess oligohydramnios?

A
  • USS to assess liquor volume
  • CTG: foetal wellbeing
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10
Q

How should we manage oligohydramnios?

A
  • Term: delivery is appropriate (IOL if indicated)
  • Pre-term: monitor with serial USS for growth, liquor volume and dopplers, regular CTGs, deliver if further abnormalities arise
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11
Q

What are the complications of oligohydramnios?

A
  • Labour: Emergency C-Section, increased incidence of CTG abnormalities
  • Neonate: Pulmonary hypoplasia and limb deformities
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12
Q

Define polyhydramnios.

A

Polyhydramnios: Increased volume of amniotic fluid >95th centile or deepest pool > 8cm.

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13
Q

What are the RFs for polyhydramnios?

A
  • Idiopathic
  • Failure of foetal swallowing
  • Foetal GI tract abnormality (atresia)
  • Congenital infections
  • Foetal polyuria (diabetes)
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14
Q

How would polyhydramnios present?

A

Symptoms of underlying cause, maternal discomfort

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15
Q

How should we investigate polyhydramnios?

A
  • USS: Diagnosis and assessment of liquor volume, foetal growth, umbilical artery doppler, exclude foetal anomalies
  • Other: exclude maternal diabetes
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16
Q

How do we manage polyhydramnios?

A
  • Ante-natal monitoring
  • Amnioreduction: if causing a problem
  • Cyclo-oxygenase inhibitor: used to reduced foetal urine output
  • Optimise diabetes control
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17
Q

What are the complications of polyhydramnios?

A
  • PTL
  • Malpresentation
  • Placental abruption
  • Cord prolapse
  • Complications of underlying pathology
  • PPH
  • Increased risk of C-section
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18
Q

Define small for gestational age.

A

Small-for-gestational age (SGA) refers to an infant born with a birth weight less than the 10th centile.

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19
Q

What are the causes of SGA?

A
  • Maternal:
    • HT
    • pre-eclampsia
    • diabetes
    • drugs
    • renal disease
    • thrombophilia
    • maternal age
    • pemphigoid gestionis
  • Foetal
    • chromosomal abnormality
    • infection (CMV, rubella)
    • multiple pregnancy
  • Other: Placental Insufficiency
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20
Q

How do we classify SGA?

A
  • Symmetrical: head and body and proportionally small
    • normally early onset, seen in chromosomal abnormalities
  • Asymmetrical: Typically later onset, abdominal circumference disproportionately smaller than the head
    • seen with placental insufficiency
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21
Q

How common are SGAs?

A

3-5% of pregnancies

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22
Q

What are the RFs for SGA?

A
  • Previous SGA baby
  • Obesity
  • Smoking
  • Diabetes
  • Existing hypertension
  • Pre-eclampsia
  • Older mother (over 35 years)
  • Multiple pregnancy
  • Low pregnancy‑associated plasma protein‑A (PAPPA)
  • Antepartum haemorrhage
  • Antiphospholipid syndrome
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23
Q

How do we assess foetal size in SGA?

A

Symphysis-fundal height

  • Serial measurement at each antenatal appt from 24 weeks improves prediction of SGA neonate
  • Plot SFH on customised chart (ethnic group, weight, height and parity)
  • Refer women in whom SFH measurement is inaccurate (BMI>35, large fibroids, hydramnios) for serial growth USS

Best method for detecting SGA and FGR

  • Fetal abdominal circumference or estimated fetal weight <10th centile

USS:

  • Umbilical Artery Doppler - abnormal if end diastolic flow absent or reversed
  • Liquor volume
  • Anomaly scan
  • Middle cerebral artery doppler (may show redistribution of blood to brain)

CTG

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24
Q

Define Severe SGA.

A

Fetus below 3rd centile

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25
Q

Low birth weight

A

BW of less than 2500 g

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26
Q

What are the 2 causes of SGA?

A
  • Constitutionally small - growing appropriately on the growth chart
  • Fetal growth restriction - IUGR → small foetus due to a pathology reducing the amount of nutrients and oxygen being delivered to the foetus through the placenta
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27
Q

What are the causes of FGR?

A
  • Placenta mediated
  • Non-placenta mediated (usually genetic or structural abnormality)
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28
Q

What are the placenta mediated growth restriction causes?

A
  • Idiopathic
  • Pre-eclampsia
  • Maternal smoking
  • Maternal alcohol
  • Anaemia
  • Malnutrition
  • Infection
  • Maternal health conditions
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29
Q

What are the non-placenta mediated growth restriction causes?

A
  • Genetic abnormalities
  • Structural abnormalities
  • Fetal infection
  • Errors of metabolism
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30
Q

What are other signs of FGR?

A
  • Reduced amniotic fluid volume
  • Abnormal Doppler studies
  • Reduced fetal movements
  • Abnormal CTGs
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31
Q

What are the complications of FGR?

A

Short term complications of fetal growth restriction include:

  • Fetal death or stillbirth
  • Birth asphyxia
  • Neonatal hypothermia
  • Neonatal hypoglycaemia

Growth restricted babies have a long term increased risk of:

  • Cardiovascular disease, particularly hypertension
  • Type 2 diabetes
  • Obesity
  • Mood and behavioural problems
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32
Q

What are the minor and major risks of SGA? How does it change monitoring?

A
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33
Q

How do we manage an SGA pregnancy?

A

The critical management steps are:

  • Identifying those at risk of SGA
  • Aspirin is given to those at risk of pre-eclampsia
  • Treating modifiable risk factors (e.g. stop smoking)
  • Serial growth scans to monitor growth
  • Early delivery where growth is static, or there are other concerns

When a fetus is identified as SGA, investigations to identify the underlying cause include:

  • Blood pressure and urine dipstick for pre-eclampsia
  • Uterine artery doppler scanning
  • Detailed fetal anatomy scan by fetal medicine
  • Karyotyping for chromosomal abnormalities
  • Testing for infections (e.g. toxoplasmosis, cytomegalovirus, syphilis and malaria)
  • Intrapartum
    • Abnormalities in umbilical artery doppler or MCA doppler: delivery by 37 weeks
    • SGA with umbilical artery AREDV <32 weeks: delivery by 32 weeks after completion of steroids

IOL can be offered with continuous CTG once contractions begin but high conversion to EMCS

34
Q

Define large for gestational age.

A
  • >4.5kg (macrosomic)
  • > 90th central EFW
35
Q

What are the causes of macrosomia?

A
  • Constitutional
  • Maternal diabetes
  • Previous macrosomia
  • Maternal obesity or rapid weight gain
  • Overdue
  • Male baby
  • Syndromes - Beckmanwith-Wiedemann
36
Q

What are the investigations for large for dates pregnancies?

A
  • OGTT (GDM)
  • Bloods (serum HCG)
  • US (liquor volume)
  • Genetic testing
37
Q

How should we manage large for dates pregnancies?

A

Most women with large for gestational age pregnancy will have a successful vaginal delivery. NICE guidelines (2008) advise against induction of labour only on the grounds of macrosomia.

38
Q

What are the complications for large for dates pregnancies?

A

The risks to the mother include:

  • Shoulder dystocia
  • Failure to progress
  • Perineal tears
  • Instrumental delivery or caesarean
  • Postpartum haemorrhage
  • Uterine rupture (rare)

The risks to the baby include:

  • Birth injury (Erbs palsy, clavicular fracture, fetal distress and hypoxia)
  • Neonatal hypoglycaemia
  • Obesity in childhood and later life
  • Type 2 diabetes in adulthood
39
Q

How do we lower the risk from shoulder dystocia?

A

The risks at delivery can be reduced by:

  • Delivery on a consultant lead unit
  • Delivery by an experienced midwife or obstetrician
  • Access to an obstetrician and theatre if required
  • Active management of the third stage (delivery of the placenta)
  • Early decision for caesarean section if required
  • Paediatrician attending the birth
40
Q

Define rhesus disease.

A
  • Development of rhesus antibodies in a rhesus negative mother after exposure to Rh +ve RBCs. Always a Rh mother.
41
Q

What causes rhesus disease?

A

Needs a sensitising event.

In subsequent pregnancies involving a RhD-positive foetus, maternal IgG antibodies will cross the placenta, forming complexes with RhD on foetal erythrocytes and destroying them.

42
Q

How would rhesus disease present?

A

Picked up on routine testing.

Can lead to hydrops fetalis

43
Q

What sensitising events can occur?

A
  • Amniocentesis, chorionic villus biopsy and cordocentesis
  • Antepartum haemorrhage/Uterine (PV) bleeding in pregnancy
  • ECV
  • Abdo trauma
  • Ectopic
  • Evacuation of molar pregnancy
  • Intrauterine death and still birth
  • Miscarriage
  • TOP
  • Delivery
  • Intra-operative cell salvage
44
Q

How do we manage rhesus disease?

A
  • Prevention: Anti- D immunoglobulin prophylaxis recommended for RhD -ve mothers at 28 and 34 weeks
  • Anti-D Ig should be administered within 72hrs of any sensitising event:
    • <12 weeks 250IU only for ectopic, TOP, molar and abnormal heavy uterine bleeding
    • 12-20 weeks 250IU
    • 20+ weeks 500IU + Kleihauer test (done to see how much fetal blood has passed into maternal blood stream)
  • If isoimmunisation has occurred, then blood transfusion for the foetus may be required
45
Q

How does the Kleihauer test work?

A

The Kleihauer test involves adding acid to a sample of the mother’s blood. Fetal haemoglobin is naturally more resistant to acid, so that they are protected against the acidosis that occurs around childbirth. Therefore, fetal haemoglobin persists in response to the added acid, while the mothers haemoglobin is destroyed. The number of cells still containing haemoglobin (the remaining fetal cells) can then be calculated.

46
Q

How has the incidence of Pulmonary embolisms changed?

A

Pulmonary embolism (PE) remains a leading direct cause of maternal death in the UK. There has been a significant fall in the maternal mortality rate from PE

47
Q

How does the risk of VTE change throughout pregnancy?

A
  • Many fatal antenatal VTE events occur in the first trimester and therefore prophylaxis for women with previous VTE should begin early in pregnancy
  • The risk for VTE increases with gestational age, reaching a maximum just after delivery
  • Caesarean section is a significant risk factor
  • The absolute risk peaked in the first 3 weeks postpartum
48
Q

What are the risk factors for VTE in pregnancy?

A
49
Q

How often should patients be risk assessed for VTE?

A
  • All women should undergo a documented assessment of risk factors for VTE in early pregnancy or prepregnancy.
  • Risk assessment should be repeated if the woman is admitted to hospital for any reason or develops other intercurrent problems.
  • Risk assessment should be repeated again intrapartum or immediately postpartum.
50
Q

How should we manage at risk women antenatally

A
  • Women with previous VTE should be offered prepregnancy counselling and a prospective management plan for thromboprophylaxis in pregnancy made. Those who become pregnant before receiving such counselling should be referred at the earliest opportunity in pregnancy to a clinician with expertise in thrombosis in pregnancy.
  • Women with previous VTE (except those with a single previous VTE related to major surgery and no other risk factors) should be offered thromboprophylaxis with LMWH throughout the antenatal period.
  • Any woman with four or more current risk factors (other than previous VTE or thrombophilia) should be considered for prophylactic LMWH throughout the antenatal period and will usually require prophylactic LMWH for 6 weeks postnatally but a postnatal risk reassessment should be made.
  • Any woman with three current risk factors (other than previous VTE or thrombophilia) should be considered for prophylactic LMWH from 28 weeks and will usually require prophylactic LMWH for 6 weeks postnatally but a postnatal risk reassessment should be made.
51
Q

How should we manage patients who have had a thrombophilia-associated VTE?

A
  • Women with previous VTE associated with antithrombin deficiency (who will often be on long-term oral anticoagulation) should be offered thromboprophylaxis with higher dose LMWH (either 50%, 75% or full treatment dose) antenatally and for 6 weeks postpartum or until returned to oral anticoagulant therapy after delivery.
  • Management should be undertaken in collaboration with a haematologist with expertise in thrombosis in pregnancy and consideration given to antenatal anti-Xa monitoring and the potential for antithrombin replacement at initiation of labour or prior to caesarean section.
  • If anti-Xa levels are measured, a test that does not use exogenous antithrombin should be used and 4-hour peak levels of 0.5–1.0 iu/ml aimed for.
  • Other heritable thrombophilic defects are lower risk and can be managed with standard doses of thromboprophylaxis.
52
Q

How should we manage VTE risk in APS?

A

Women with VTE associated with the antiphospholipid syndrome (APS) (who will often be on longterm oral anticoagulation) should be offered thromboprophylaxis with higher dose LMWH (either 50%, 75% or full treatment dose) antenatally and for 6 weeks postpartum or until returned to oral anticoagulant therapy after delivery.

Pregnant women with APS and prior VTE or arterial thromboses should be managed in collaboration with a haematologist and/or rheumatologist with expertise in this area

53
Q

When should thromboprophylaxis be started?

A
  • Antenatal thromboprophylaxis for those with previous VTE should begin as early in pregnancy as practical.
  • Women without previous VTE and without particular first trimester risk factors or admission to hospital, but with four other risk factors, should be considered for antenatal prophylaxis throughout pregnancy.
  • Women without previous VTE and without particular first trimester risk factors or admission to hospital, but with three other risk factors, can start antenatal prophylaxis at 28 weeks of gestation.
54
Q

What are the 1st trimester RFs for VTE?

A
  • Women admitted with hyperemesis should be considered for thromboprophylaxis with LMWH and can discontinue thromboprophylaxis when the hyperemesis resolves.
  • Women with ovarian hyperstimulation syndrome should be considered for thromboprophylaxis with LMWH in the first trimester.
  • Women with an IVF pregnancy and three other risk factors should be considered for thromboprophylaxis with LMWH starting in the first trimester.
55
Q

When should thromboprophylaxis be interrupted for delivery?

A
  • Women receiving antenatal LMWH should be advised that if they have any vaginal bleeding or once labour begins they should not inject any further LMWH
  • Regional techniques should be avoided if possible until at least 12 hours after the previous prophylactic dose of LMWH. (24 for therapeutic dose)
  • LMWH should not be given for 4 hours after use of spinal anaesthesia or after the epidural catheter has been removed and the catheter should not be removed within 12 hours of the most recent injection.
    *
56
Q

When should LMWH be given if a c-section is happening?

A

Women receiving antenatal LMWH having an elective caesarean section should receive a thromboprophylactic dose of LMWH on the day prior to delivery and, on the day of delivery, any morning dose should be omitted and the operation performed that morning

57
Q

How soon after delivery should LMWH be given?

A
  • The first thromboprophylactic dose of LMWH should be given as soon as possible after delivery provided there is no postpartum haemorrhage and regional analgesia has not been used.
  • Women at high risk of haemorrhage with risk factors including major antepartum haemorrhage, coagulopathy, progressive wound haematoma, suspected intra-abdominal bleeding and postpartum haemorrhage may be managed with anti-embolism stockings (AES), foot impulse devices or intermittent pneumatic compression devices. Unfractionated heparin (UFT) may also be considered
  • Thromboprophylaxis should be started or reinstituted as soon as the immediate risk of haemorrhage is reduced.
58
Q

What are the risk factors for VTE after delivery?

A
  • All women with class 3 obesity (BMI greater than or equal to 40 kg/m2 ) should be considered for prophylactic LMWH in doses appropriate for their weight for 10 days after delivery.
  • Women with two or more persisting risk factors should be considered for LMWH in prophylactic doses appropriate for their weight for 10 days after delivery.
  • All women with a previous history of confirmed VTE should be offered thromboprophylaxis with LMWH or warfarin for at least 6 weeks postpartum regardless of the mode of delivery.
  • Women with a family history of VTE and an identified thrombophilia should be considered for 6 weeks’ postnatal thromboprophylaxis.
  • All women who have had caesarean sections should be considered for thromboprophylaxis with LMWH for 10 days after delivery apart from those having an elective caesarean section who should be considered for thromboprophylaxis with LMWH for 10 days after delivery if they have any additional risk factors
59
Q

Which women should not be given thromboprophylaxis with LMWH?

A

Further advice on the management of a woman with both VTE risk factors and bleeding risk factors or LMWH allergy may be sought from a haematologist with expertise in the management of thrombosis and bleeding disorders in pregnancy.

60
Q

How common is substance use disorder in pregnancy?

A
  • 6000 births to a drug user per year
  • Common to have psychiatric comorbidity
61
Q

What should we screen for in a patient with substance use?

A
  • Social Problems
    • Housing
    • Crime
    • Other children abused
  • Co-existent addictions
  • Malnutrition: especially iron, Vit B and C
  • Risk of viral infection: HIV, hep b
62
Q

What are the complications of alcohol use in pregnancy?

A
  • increased risk of miscarriage
  • still birth and infant mortality
  • congenital anomalies
  • low birthweight
  • reduced gestational age
  • preterm delivery
  • Associated with foetal alcohol spectrum disorders
63
Q

What are the complications of smoking use in pregnancy?

A
  • damage to umbilical cord structure
  • miscarriage
  • increased risk of ectopic
  • low birth weight
  • placental abruption
  • preterm birth
64
Q

What are the complications of cannabis use in pregnancy?

A
  • linked with preterm labour
  • low BW
  • small for gestational age
  • adverse consequences for foetal and adolescent brain
  • poorer academic achievement
65
Q

What are the complications cocaine use in pregnancy?

A

premature rupture of membranes

placental abruption

preterm birth

low BW

66
Q

What are the complications opioids use in pregnancy?

A
  • low BW
  • resp problems
  • 3rd trimester bleeding
  • neonatal abstinence syndrome (post natal withdrawal)
67
Q
A

Line nigra

68
Q
A

Striae gravidarum

69
Q
A

Striae albicans

70
Q
A

Pemphigoid Gestationis

71
Q

What is pemphigoid gestationis? When does it present? How does it change? How do we manage it? What is it associated with?

A
  • a rare (1 in 60 000 pregnancy) pruritic auto-immune bullous disorder.
  • Presents late in 2nd or 3rd trimester starting on the abdomen (50% of cases) and progresses to widespread clusters of blisters which spare the face.
  • Management aims to relieve pruritis and prevent new blister formation, and is achieved through the use of potent topical steroids and/ or oral prednisolone
  • association with preterm delivery and small for gestational age births, but no increase in pregnancy loss

It also recurs in most subsequent pregnancies

72
Q
A

Polymorphic eruption of pregnancy

73
Q

What is Polymorphic eruption of pregnancy? When does it present? Where does it occur and where does it extend? How do we manage it?

A
  • self-limiting pruritic inflammatory disorder -
  • usually presents in 3rd trimester and/ or immediately post-partum.
  • Often occurs on lower abdomen on striae and extends to thigh, buttocks, legs and arms, while sparing the umbilicus and rarely involving the face, feet and hands.
  • Resembles toxic erythema.
  • Tx: symptomatic treatment is sufficient
74
Q
A

Prurigo of pregnancy

75
Q

What is Prurigo of pregnancy? How, where and when does it present? When does it resolve? What is tx?

A
  • (1 in 300)
  • is simply a common pruritic disorder.
  • Looks like excoriated papules on extensor limbs, abdomen and shoulders.
  • Usually starts around 25-30 weeks of pregnancy and resolves after delivery.
  • Tx: symptomatic with topical steroids and emollients
76
Q
A

Pruritic folliculitis

77
Q

What is Pruritic folliculitis? What parts does it affctect? How do we manage it?

A
  • pruritic follicular eruption with papules and pustules that mainly affect the trunk but can affect the limbs.
  • Tx: Topical steroids
78
Q

Define mastitis.

A

Mastitis refers to inflammation of breast tissue, and is a common complication of breastfeeding. It can occur with or without associated infection.

79
Q

What causes mastitis?

A

Mastitis can be caused by obstruction in the ducts and accumulation of milk. Regularly expressing breast milk can help prevent this occurring.

Mastitis can also be caused by infection. Bacteria can enter at the nipple and back-track into the ducts, causing infection and inflammation. The most common bacteria is staph aureus.

80
Q

How does mastitis present?

A
  • Breast pain and tenderness (unilateral)
  • Erythema in a focal area of breast tissue
  • Local warmth and inflammation
  • Nipple discharge
  • Fever
81
Q

How do we manage mastitis?

A

Where mastitis is caused by blockage of the ducts, management is conservative:

  • continued breastfeeding
  • expressing milk
  • breast massage.
  • Heat packs, warm showers and simple analgesia can help symptoms.

When conservative management is not effective, or infection is suspect (e.g. the woman is febrile), antibiotics should be started.

  • Flucloxacillin is first line, or erythromycin if allergic to penicillin.
  • A sample of milk can be sent to the lab for culture and sensitivities.
  • Fluconazole may be used for suspected candidal infections.
  • Women should be encouraged to continue breastfeeding, even when infection is suspected.
    • It will not harm the baby and will help to clear the mastitis by encouraging flow. Where breastfeeding is difficult, or there is milk left after feeding, they can express milk to empty the breast.

A rare complication if not adequately treated, is a breast abscess. This may need surgical incision and drainage.

82
Q

What causes candida of the nipple? How do we manage it?

A

Candidal infection of the nipple can occur, often after a course of antibiotics. This can lead to recurrent mastitis, as it causes cracked skin on the nipple that create an entrance for infection. It is associated with oral thrush and candidal nappy rash in the infant.

Both the mother and baby need treatment, or it will reoccur. Treatment is with:

  • Topical miconazole 2% after each breastfeed
  • Treatment for the baby (e.g. miconazole gel or nystatin)

Obstetrics (7 decks)

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