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Obstetrics > Maternal Complications > Flashcards

Maternal Complications Flashcards

1
Q

What are the causes of sudden maternal collapse?

A

Neurological:

  • Pre-eclampsia (with seizures)
  • Intracranial haemorrhage

Thoracic:

  • Anaphylaxis
  • Pulmonary embolism
  • Amniotic fluid embolism
  • Aortic dissection
  • Cardiac causes: MI, arrhythmias, cardiomyopathy, syncope

Abdominal:

  • Hypoglycaemia
  • Sepsis
  • Haemorrhage: uterine, hepatic, splenic

Drugs:

  • Magnesium sulphate
  • Local anaesthetic given IV
  • Illicit drugs
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2
Q

What is the epidemiology surrounding sudden maternal collapse and death?

A

Thromboembolism is the most common cause of direct maternal death

Haemorrhage is the most common cause of maternal collapse

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3
Q

What is the management protocol for sudden maternal collapse in a non-hospital setting?

A

Take and ABC approach, get help, and begin CPR immediately if required.

For pregnant women above 20 weeks, tilt them to the left to relieve the pressure of the gravid uterus on the IVC and aorta

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4
Q

What is the management protocol for sudden maternal collapse in a hospital setting?

A

Take an ABC approach, and get help.

Airways: intubate
Breathing: give oxygen via breathing bag until intubated
Circulation: Commence CPR immediately if not breathing and insert an IV

Volume: aggressive approach but be careful in cases of pre-eclampsia and eclampsia

Perform an abdominal US to find cause of haemorrhage.

Delivery achieved within 5 minutes if CPR is not working.

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5
Q

What antiepileptic medications are contraindicated in pregnancy?

A

Sodium valproate must not be used

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6
Q

What antiepileptic medication can be used during pregnancy?

A

First line: Lamotrigine

Carbamazepine may also be used

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7
Q

What contraceptive advice should be given to women with epilepsy?

A

Anti-convulsant medications are cytochrome P450 inducers so lower the efficacy of oral contraceptives.

They should be advised to use depot injections, the copper IUS or the mirena coil.

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8
Q

What is the association between anti-convulsant medications and congenital abnormalities?

A

There is some associated risk of congenital malformations and neurodevelopmental defects.

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9
Q

What pre-conception advise must be given to women with epilepsy?

A

The medication must first be optimised.

  • Use the lowest possible effective dose, and minimise the number of therapies taken.
  • Stop sodium valproate

Supplements:
- Folic acid at 5mg every day from pre-conception to 12 weeks pregnancy

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10
Q

What antenatal care is given to women with epilepsy?

A

The normal USS for structural abnormalities is conducted at 18-20 weeks.

Foetal growth should be monitored for some anti-convulsant medication (topiramate)

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11
Q

What post-natal advice should be given to women with epilepsy?

A
  • Vitamin K injections should be given to the neonate to prevent haemorrhages associated with AEDs
  • Breastfeeding is safe and should be encouraged
  • Women taking phenobarbital and benzodiazepines may see some drowsiness in their breastfed children
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12
Q

What is the epidemiology surrounding pre-existing hypertension in pregnant ladies?

A

This affects around 1-3% of all pregnant women

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13
Q

What are the changes in physiology during pregnancy in regards to blood pressure?

A

There is a fall during the 2nd trimester. However, BP levels rise back to pre-pregnancy levels in the 3rd trimester

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14
Q

What are the complications of pre-existing hypertension in pregnancy?

A

Maternal:

  • 6 times more likely to develop pre-eclampsia
  • Placental abruption
  • Heart failure
  • Intra-cranial haemorrhage (rare)

Foetal:
- Growth restriction due to placental insufficiency

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15
Q

What investigations are performed in a case of pre-existing hypertension in pregnancy?

A

Exclude secondary hypertension:
- Blood tests, renal USS, echo, 24 hour urine

To prevent pre-eclampsia from developing:
- Regular BP checks

To monitor foetal growth:
- Serial growth scans

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16
Q

How is pre-existing hypertension managed in pregnancy?

A

First line: labetalol
Second line: methyl dopa

DO NOT use ACE inhibitors or diuretics

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17
Q

What hypertensive medications are contraindicated in pregnancy? Which are indicated?

A

Contraindicated:

  • ACE inhibitors
  • Diuretics

Indicated:
- Beta blockers

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18
Q

What is pregnancy-induced hypertension?

A

This is new onset hypertension of >140/90mmHg during pregnancy (after 20 weeks), in the absence of significant proteinuria or features of pre-eclampsia.

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19
Q

What is the epidemiology surrounding pregnancy-induced hypertension?

A

This affects 4-8% of pregnant women

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20
Q

What are the complications of pregnancy-induced hypertension?

A

These are the same as pre-existing hypertension:

Maternal:

  • Increased risk of pre-eclampsia
  • Placental abruption
  • Haemorrhage
  • Heart failure

Foetal:
- Growth restriction

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21
Q

What are the investigations performed in a case of pregnancy-induced hypertension?

A
  • Regular BP checks
  • Urine analysis for proteinuria
  • Regular growth scans for the foetus
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22
Q

What is the management of pregnancy-induced hypertension?

A

Do not treat unless the blood pressure is above 150/100mmHg

First line: labetalol
Second line: methyldopa

DO NOT USE ACE INHIBITORS

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23
Q

What is pre-eclampsia?

A

This is a multisystem disorder, characterised by:

  • A blood pressure of over 140/90mmHg on two occasions at least 4 hours apart
  • A 24 hour urine protein collection of over 300mg

It usually arises after wk20 and resolves after pregnancy

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24
Q

How do you classify cases of pre-eclampsia?

A

According to the blood pressure:

  • Mild: >140/90mmHg
  • Moderate: >150/100mmHg
  • Severe: >160/110mmHg
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25
Q

What is the epidemiology of pre-eclampsia?

A

It affects around 6% of nulliparous women

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26
Q

What are the risk factors associated with pre-eclampsia?

A
  • Nulliparity
  • Previous pre-eclampsia or FHx
  • New partner
  • Long interval from last pregnancy (>10 years)
  • Obesity
  • Increasing maternal age
  • Diabetes
  • Pre-existing hypertension
  • Pre-existing renal damage
  • Multiple pregnancy
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27
Q

What is the pathophysiology of pre-eclampsia?

A

While this is not totally understood, it is believed to be part of placental implantation, and the symptoms are as a result of maternal vascular endothelial damage.

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28
Q

What are the clinical features of pre-eclampsia?

A

Symptoms:

  • Can be asymptomatic
  • Headaches and drowsiness
  • Visual disturbances
  • Epigastric pain
  • Nausea and vomiting

Signs:

  • Hypertension
  • Oedema
  • Hyperreflexia and clonus
  • Proteinuria on urinalysis
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29
Q

What are the complications of pre-eclampsia?

A

Complications can be predicted by the presence or absence of placental growth factor (PlGF) which is part of the family of vascular endothelial growth factors (VEGF). Low levels of PlGF may predict adverse outcomes in pregnancies with pre-eclampsia. Full trial results are awaited.

Maternal:

  • Eclampsia (tonic/clonic seizures due to cerebrovascular vasospasm)
  • Cerebrovascular haemorrhage
  • HELLP syndrome (haemolysis, elevated liver enzymes, low platelets)
  • DIC
  • Renal failure
  • Pulmonary oedema
  • Placental abruption

Foetal:

  • IUGR
  • Pre-term delivery
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30
Q

What investigations are performed in a case of pre-eclampsia?

A

Maternal:

  • FBC, U&Es, LFTs
  • BP checks

Diagnosis:

  • Urinalysis and 24 hour urine collection
  • FBC (platelets) and U&Es (renal function) and LFTs (lactate dehydrogenase associated with haemolysis)

Foetal:

  • Serial growth scans
  • Umbilical artery doppler
  • CTG
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31
Q

How is pre-eclampsia managed?

A

Medication:

  • Only if blood pressure is >160/110mmHg
  • First line: labetalol
  • Second line: nifedipine

Magnesium sulphate used to prevent or treat eclampsia (increases cerebral perfusion and reduces oedema)
- Corticosteroids: considered before 34 weeks for foetal lung maturity

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32
Q

What must be monitored when treating pre-eclampsia with magnesium sulphate?

A

Magnesium sulphate toxicity:

  • This presents first as reduced tendon reflexes
  • Can progress to respiratory depression, hypotension and renal impairment
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33
Q

What indications are there to admit a woman with pre-eclampsia?

A
  • Symptomatic pre-eclampsia
  • Proteinuria
  • Severe hypertension (>160/110mmHg)
  • Foetal compromise
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34
Q

How is delivery in a case of pre-eclampsia managed?

A

The timing and method depends on the maternal and foetal wellbeing.

If <34 weeks:

  • Corticosteroids administered
  • C-section

If >34 weeks:

  • Consider vaginal delivery
  • IOL possible and epidural will reduce the BP
  • Monitor foetal health with a CTG and administer anti-hypertensives
  • If maternal BP is above 170/110mmHg, discourage pushing
  • 3rd stage of labour: give Syntocinon
  • Do not give ergometrine (can increase BP)
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35
Q

What is the definitive cure for pre-eclampsia/eclampsia?

A

The delivery of the placenta

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36
Q

What is gestational diabetes mellitus?

A

This is any insulin resistance that is onset during pregnancy

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37
Q

What is the epidemiology surrounding gestational diabetes mellitus?

A

It effects 2-4% of women

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38
Q

What is the pathophysiology surrounding gestational diabetes mellitus?

A

Pregnancy causes a more insulin resistant state, due to human placental lactogen, and a higher glucose to nourish the child. This can contribute to an overall hyperglycaemic state.

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39
Q

What are the risk factors for gestational diabetes mellitus?

A
  • BMI >30
  • Ethnicity (Asian, African, middle-eastern)
  • Previous GDM
  • Previous big baby >4.5kg
  • 1st degree relative with diabetes
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40
Q

What is the diagnostic criteria for gestational diabetes mellitus?

A
  • Fasting glucose of >5.6mmol/L

- 75g Glucose tolerance test two hour levels of >7.8mmol/L

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41
Q

What is the management algorithm for gestational diabetes mellitus?

A

Monitoring:

  • Measure blood glucose 7 times a day (pre and post meals, night time)
  • Should be <5.3mmol/L fasting, <7.8mmol/L 1-hour post meal, <6.4mmol/L 2-hour post meal
  • Should be >4mmol/L at all times (if on insulin)

Conservative management

  • Diet and exercise
  • Weight loss

Medical management

  • Metformin
  • Insulin

Foetal monitoring:

  • Serial growth scan every 4 weeks from week 38
  • Routine foetal wellbeing assessment is not recommended

Birth
- Advised to give birth no later than 40+6

Post-partum care

  • Assess for neonatal hypoglycaemia
  • Offer OGTT at 6 weeks to assess diabetes
  • Screen annually for diabetes
  • Breastfeeding is safe on metformin
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42
Q

What investigations are performed in a case of gestational diabetes mellitus?

A
  • 75g oral glucose tolerance test for all at-risk women at weeks 24-28
  • If previous GDM, 75g OGTT performed at 16 weeks, or at booking.
  • HbA1C measurement at diagnosis to assess pre-existing diabetes
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43
Q

What are the complications of gestational diabetes mellitus?

A
  • Macrosomia
  • Shoulder dystocia
  • Neonatal hypoglycaemia (usually self-limiting)

Increased risk of still birth

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44
Q

What are the normal levels for the 75g oral glucose tolerance test?

A

Fasting: <6 mmol/L
1 hour: <10 mmol/L
2 hours: <7.8 mmol/L

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45
Q

How can you classify different levels of gestational diabetes mellitus?

A

Type A1: abnormal fasting, normal 2 hours

Type A2: abnormal 2 hours

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46
Q

For women with pre-existing diabetes, what is the pre-conception advise that should be given?

A

Advice

  • Do not conceive if HbA1C is >86
  • Keep HbA1C at <48 to reduce risks to foetus
  • Education programme

Assessment:

  • Renal assessment
  • Retinal assessment

Medications:

  • Metformin safe to use in pregnancy
  • Discontinue ACE inhibitors and ARBs

Supplements:
- Folic acid supplements: 5mg a day until 12 weeks

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47
Q

For women with pre-existing diabetes, what are the investigations performed during pregnancy?

A

Retinal assessment:

  • At booking (unless within 3 months)
  • If retinopathy present, again at 16-20 weeks
  • If no retinopathy, again at 28 weeks

Renal assessment:

  • At booking (unless within 3 months)
  • If proteinuria >5mg/day, consider thromboprophylaxis
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48
Q

How is birth managed in a woman with diabetes?

A

Timing of birth:

  • Most women offered elective births at 38-40 weeks
  • Advised to give birth by 40+6 weeks

During labour:

  • Glucose should be monitored and kept at 4-7 mmol/L
  • Consider sliding scale if glucose control is poor

After birth:

  • Foetal monitoring of blood glucose
  • Breastfeeding is encouraged
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49
Q

For a woman with gestational diabetes/diabetes, what should be considered when administering corticosteroids for per-term delivery?

A

Insulin dose must increase accordingly to steroid use

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50
Q

What is antepartum haemorrhage?

A

This is vaginal bleeding after the 24th week of pregnancy (sometimes defined at 20 weeks)

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51
Q

What is the epidemiology surrounding antepartum haemorrhage?

A

This occurs in 4-5% of pregnancies

52
Q

What are the causes of antepartum haemorrhage?

A

Bloody show

Placental causes:

  • Placental abruption
  • Placenta praevia
  • Vasa praevia

Local causes:

  • Cervicitis
  • Cervical carcinoma
  • Vaginal infection/trauma/lesions
53
Q

What is a bloody show?

A

It is a small amount of blood and mucus that is discharged near the end of pregnancy. It is a sign that labour is imminent.

54
Q

What is placental abruption?

A

This is the premature detachment of the placenta from the uterine wall

55
Q

What is the epidemiology surrounding placental abruption?

A

It occurs in 1 in 120 pregnancies

56
Q

What are the risk factors associated with placental abruption?

A
  • Hypertension
  • Uterine expansion (multiple pregnancy, polyhydramnios)
  • Trauma
  • Hx of abruption
  • Uterine anomaly (fibroids)
57
Q

How can placental abruptions be classified?

A
  • Revealed (80%) where there is bleeding

- Concealed (20%) where the bleeding is contained behind the placenta

58
Q

What are the clinical features of placental abruption?

A

Symptoms:

  • Vaginal bleeding (80% of the time)
  • Abdominal pain
  • Foetal distress
  • Uterine contractions

Signs:

  • Shock
  • Woody, hard uterus
  • Diminished foetal heart sounds
59
Q

What investigations help determine the diagnosis?

A

Placental abruption is a clinical diagnosis; investigations are performed to assist management.

  • Monitor maternal and foetal vital signs
  • Bloods (FBC, coagulation, U&Es, crossmatch)
  • Catheter to monitor urine output
  • USS (exclude placental praevia)
60
Q

What is the management of a placental abruption?

A
  • Admit
  • IV fluids
  • Consider a blood transfusion
  • Corticosteroids (if <34 weeks)
  • Analgesia
  • Anti-D therapy if rhesus negative
61
Q

How does one manage delivery in a case of placental abruption?

A

Delivery will depend on the foetal heart rate.

If heart rate absent:
- Vaginal delivery

If present:

  • Distress: CS
  • No distress and >37 weeks: IOL
  • No distress and <34 weeks: give corticosteroids and monitor
62
Q

What are the complications associated with placental abruption?

A

Maternal:

  • Hypovolaemic shock
  • Acute renal failure
  • DIC
  • Rhesus D disease
  • Death

Foetal:

  • IUGR
  • Pre-term birth
  • Stillbirth
63
Q

Who is most at risk in placental abruption?

A

The mother

64
Q

What is placenta praevia?

A

This is a low lying placenta, diagnosed after 34 weeks gestation.

65
Q

What is the epidemiology surrounding placenta praevia?

A

This occurs 1 in 200 pregnancies

66
Q

What is the pathophysiology of placenta praevia?

A

At 20 weeks, it is common for a placenta to be low lying, as the lower segment of the uterus develops last. Only after 34 weeks, can a placenta be described as placenta praevia.

67
Q

What are the risk factors for placenta praevia?

A
  • Multiple pregnancy
  • Previous placenta praevia
  • Previous TOP
  • Previous CS
  • Previous uterine surgery/scarring
68
Q

What are the clinical features of placenta praevia?

A
  • Painless vaginal bleeding

- Foetal mal-presentation is common

69
Q

What investigations should be performed in a case of placenta praevia?

A

DO NOT PERFORM VAGINAL EXAM UNTIL PLACENTA PRAEVIA IS EXCLUDED - THIS CAN CAUSE HAEMORRHAGE

  • Transabdominal US
  • Maternal and foetal monitoring
  • Bloods: FBC, rhesus, U&Es
  • Catheterisation
70
Q

What is the management of placenta praevia?

A
  • Admit
  • Blood transfusion if necessary
  • Anti D if rhesus negative
  • Corticosteroids if <34 weeks
71
Q

How is delivery managed in placenta praevia?

A
  • Elective CS at 39 weeks

- If severe bleeding, emergency CS

72
Q

What are the maternal complications of placenta praevia?

A

Mal-invasion of the placenta into the uterine wall

73
Q

Describe different mal-invasions of the placenta into the uterine wall

A

Placenta accreta
- Placenta attaches to the myometrium rather than the decidua basalis

Placenta increate
- The placenta invades through the myometrium

Placenta percreta
- The placenta invades beyond the myometrium

The normal is termed placenta decidua

74
Q

What is vasa praevia?

A

This is where the foetal blood vessels and their memranes cover the internal os and are blow the presenting part

75
Q

What are the clinical features of vasa praevia?

A

This is usually noted antenatally, through US

If not:

  • Foetal bleeding after SROM
76
Q

What test can be done to determine if blood if foetal or maternal?

A

Apt test (haemoglobin alkaline elution test)

Foetal erythrocytes are resistant to rupture and mixture will stay red.

77
Q

What are the complications of vasa praevia?

A
  • Foetal blood is approximately 80ml per kg so the foetus can exsanguinate quickly
78
Q

What is the management of vasa praevia?

A

An emergency caesarean section

79
Q

What is an amniotic fluid embolism? What is the epidemiology involved?

A

It is amniotic fluid leaking into the maternal circulation. It is the 5th leading maternal death, with death, when an outcome, occurring within 9 hours of onset.

80
Q

What is the cause of symptoms and death in amniotic fluid embolism?

A
  • Similar to anaphylaxis reaction

- Inflammation throughout body

81
Q

What are the clinical features of amniotic fluid embolism?

A
  • Bleeding
  • Respiratory distress
  • Hypotension
  • Seizures
82
Q

What are the clinical signs of amniotic fluid embolism?

A
  • DIC

- Hypotension

83
Q

What are the risk factors for amniotic fluid embolism?

A
  • Older
  • Multiparity
  • TOP, amniocentesis
  • Abruption, trauma
  • Caesarean section
84
Q

How is amniotic fluid embolism diagnosed?

A
  • Exclusion
  • Clotting screen
  • Post mortem: foetal cells and hair in circulation
85
Q

What is the management of amniotic fluid embolism?

A
  • ABCDE approach
  • Fluids, oxygen
  • Blood products
  • Emergency caesarean section
86
Q

What can cause maternal anaemia in pregnancy, and how does it present?

A
  • Iron/folic acid deficiency
  • Thalassaemia or sickle cell
  • Coeliac disease

It presents with pallor, lethargy, dyspnoea and dizziness

87
Q

How is anaemia in pregnancy managed?

A
  • Iron replaced only if ferritin <30 at 1-200mcg a day
88
Q

What are the complications of anaemia in pregnancy?

A
  • Maternal and foetal death
  • Prematurity
  • Low birth weight
  • Foetal complications
89
Q

What are the considerations in thalassaemia and sickle cell in pregnancy?

A

Thalassaemia:

  • Father tested and genetic counselling
  • CVS and umbilical cord bloods to test and offer TOP

Sickle cell:

  • FBC tested at 20, 28 and 32 weeks
  • If Hb <60, consider transfusion
  • Offer 5mg daily folate
  • Prophylactic antibiotics during and after pregnancy
  • Treat crisis with heparin

Complications of sickle cell:

  • Spontaneous abortion
  • Pre-term delivery and low birth weight
  • Stroke, PE, UTIs
  • Pregnancy induced HTN
90
Q

What considerations are taken for women with asthma in pregnancy?

A

1/3 will have improved symptoms, 1/5 need emergency treatment and 2/3 of those need admission

  • All medications are safe for pregnancy and breastfeeding
  • Pre-pregnancy optimisation is necessary and continued medication throughout
  • In exacerbations, treat vigorously and keep SaO2 at >95%
91
Q

What is hyperemesis gravidarum? What are the features of it? What are the risk factors?

A

It is severe vomiting, associated with a 5% weight loss, dehydration, electrolyte imbalance, ketosis and hospital admission. It affects less than 1 % of pregnancies.

The risks have been outlined as female babies, multiple pregnancies. Smoking and maternal age >30 are protective.

92
Q

What is the management of hyperemesis gravidarum? What are the complications?

A

Management:

  • Diet, fluids and electrolytes
  • Vitamins (thiamine)
  • Thromboprophylaxis (LMWH)
  • Avoid anti-emetics but if needed, promethazine

Complications:

  • Maternal: weight loss, hypernatraemia, acidosis, Mallory-Weiss tear, retinal haemorrhage
  • Foetal: low birth weight
93
Q

What is obstetric cholestasis? What are the risk factors and how does it present?

A

It is an intense pruritus, associated with deranged LFTs (AST and ALT elevation). Risk factors include a past history of OC, a family history of OC, multiple pregnancy, gallstones and hepatitis C infection.

OC presents in the third trimester, with intense itching, particularly in the palms and soles.

94
Q

How is obstetric cholestasis diagnosed? How is it managed? What are the complications?

A

OC is a diagnosis of exclusion, and one must exclude EBV, CMV, pre-eclampsia and acute fatty liver of pregnancy.

Management surround three main aspects:
Monitoring:
- LFTs monitored weekly from diagnosis
- LFTs should remain the same throughout pregnancy
- Check again 10 days post delivery

Treatment:

  • Ursodeoxycholic acid used for pruritus
  • Vitamin K sometimes offered

Delivery:

  • Main resolution of symptoms
  • IOL considered past 37 weeks

Complications:

  • Foetal distress risk and intrauterine death
  • Risk of prematurity
95
Q

What is acute fatty liver of pregnancy? What is the epidemiology associated?

A

An occurrence usually in late pregnancy, it is a rare condition causing fatty liver in pregnancy. It occurs 5:100,000 and risk factors include pre-eclampsia, multiple pregnancies and male foetuses.

96
Q

How does acute fatty liver of pregnancy present? How is it investigated?

A

Acute presentation with nausea and vomiting, abdominal pain, fevers, headache and pruritus; this all typically starts after 35 weeks.

Investigate with a FBC (high WCC, low platelets), LFTs (high AST and ALT, high bilirubin, abnormal clotting)

97
Q

How is acute fatty liver of pregnancy managed? What are the complications?

A

Management:

  • Consider early delivery
  • Condition usually resolves with delivery

Complications:

  • 1.8% maternal and 23% foetal mortality rate
  • DIC and GI bleeding
  • Hepatic coma
  • AKI and pancreatitis
98
Q

What are the normal thyroid changes in pregnancy?

A
  • Total T3 and T4 increase
  • Free T3 and T4 stay the same
  • TSH stays the same
99
Q

How will hypothyroidism present in pregnancy? What is the management? What are the risks

A

Presentation:

  • Can be subtle and difficult to differentiate from pregnancy
  • Can be classical presentation
  • Tiredness, weakness, hair loss, intolerance to cold, sleep disturbance
  • High TSH, low T4

Management:
- Levothyroxine is safe, higher dose than normal in pregnancy
- Thyroid produces 50% more thyroxine in pregnancy
Check TSH 6-8 weeks postpartum and bring levothyroxine back to pre-pregnancy levels

Complications:

  • Congestive cardiac failure
  • Adrenal crisis, megacolon, psychosis, myxoedema coma
  • Anaemia, PIH, pre-eclampsia, placental abruption, PPH, prematurity, low birth weight, foetal death, neonatal respiratory distress
100
Q

What pre-pregnancy counselling is required for hyperthyroidism?

A
  • General advice given to all women
  • Pre-conception patients may be given definitive options (surgery or radio-iodine) - surgery method of choice
  • TSH should be <2.5
  • Adherence to medication is very important
  • Propylthiouracil is better than carbimazole (change to carbimazole in later months)
  • TRAb checked at 24-28 weeks
101
Q

What is transient gestational hyperthyroidism? How is it managed?

A
  • hCG stimulates the TSH receptor
  • Molar pregnancy
  • Anti-thyroid drugs do not help
  • Resolves as hCG falls
102
Q

What is postpartum thyroiditis?

A

Abnormal TSH levels within 12 months of delivery, in the absence of another cause
- Increased risk in those with T1DM or raised TRAb in pregnancy

103
Q

What should warrant a measured TFTs in pregnancy?

A
  • Tachycardia and palpitations
  • Heat intolerance
  • Systolic murmur
  • Bowel disturbance
  • Failure to gain weight
  • Emotional upset
  • Any signs of Grave’s
104
Q

When is neonatal hyperthyroidism a risk?

A

When TRAb is >500% of normal (checked at diagnosis and 22-26 weeks)

105
Q

What are the complications of hyperthyroidism in pregnancy?

A

maternal:

  • PIH, pre-eclampsia
  • Cardiac failure
  • Premature labour

Foetal:

  • High miscarriage risk
  • Growth restriction
  • Low birth weight
  • Still birth
  • Thyroid dysfunction
106
Q

What is the postpartum management of hyperthyroidism?

A

Maternal

  • Check TFTs at 6 weeks and 3 months
  • Continue breastfeeding

Foetal:
- Check TFTs at 6 hours and a few days

107
Q

Describe the key considerations for mothers with cardiac disease

A

Cardiac disease is the leading cause of indirect maternal deaths in the UK. The key is preconception advice and optimisation of any cardiac illness.

108
Q

Describe the considerations for mothers with pulmonary hypertension

A

This has a mortality of 25-40 percent in pregnancy. These women should be advised against pregnancy and offered a TOP.

109
Q

Describe the considerations for mothers with congenital heart disease

A

More women are surviving into adulthood and these are most commonly ASD, VSD and PDA. Refer these women to echocardiography; their children are more at risk of IUGR

110
Q

Describe the considerations for mothers with Marfan syndrome

A

Pre-conception advise is paramount here. There is a risk of aortic dissection and rupture. Root replacement should be offered before pregnancy and offer caesarean section.

111
Q

Describe the considerations for mothers with mitral stenosis

A

This can be dangerous. Advise the mother to be wary of any dyspnoea, orthopnoea or PND. Monitor the mother with echocardiograms and aggressively treat any AF. A valve area of less than 1cm^3 holds a poorer prognosis

112
Q

Describe the considerations for mothers with arrhythmias

A

Exclude more sinister diagnoses for sinus tachycardia. For supraventricular tachycardia, offer Valsalva manoeuvres and adenosine.

113
Q

Describe the considerations for mothers with artificial heart valves

A

While warfarin risks foetal harm, heparin risks valve thrombosis. Options include:

  • Warfarin throughout pregnancy
  • LMWH for wk6-12 then warfarin
  • LMWH throughout pregnancy
114
Q

Describe the considerations for mothers with ischaemic heart disease

A

Management is as for the non-pregnant woman

115
Q

Describe the considerations for mothers with peri-partum cardiomyopathy

A

This is rare and defined as heart failure without known cause either 1 month pre-partum or months post-partum. If diagnosed antenatally, offer elective delivery. Otherwise offer anticoagulants and conventional heart failure treatment.

116
Q

Describe the considerations for mothers with cardiac failure

A

Manage with diuretics, vasodilators, beta blockers and inotropes. Give ACEi only after delivery.

117
Q

How are mothers with cardiac disease managed throughout pregnancy?

A

Mothers will have regular checks by the cardiologist and will be treated to prevent anaemia, smoking and obesity. Hypertension will be treated and they will be referred for echo. Any mothers with heart failure will be admitted.

Labour has worse outcomes for those with reduced cardiac output. Aim for vaginal delivery but offer CS as per the cardiologists advice. Beware use of IV fluids. Avoid ergometrine (use oxytocin) and allow use of epidurals if hypotension can be avoided. Most cardiac deaths are in the immediate post-partum period.

118
Q

Describe the considerations of obesity in pregnancy

A

These mothers are more at risk of:

  • GDM 3x
  • Pregnancy induced hypertension and pre-eclampsia 2x
  • Venous thromboembolism 2x
  • Subfertility, miscarriage, stillbirth
  • Maternal cardiac disease
  • Failed induction, instrumental delivery, caesarean section

Management:

  • Referral to consultant-led care
  • 5mg folic acid from 1 month before conception to 12 weeks
  • 10mcg vitamin D supplementation
  • Screen for diabetes at 24-28 weeks
  • Consider LMWH thromboprophylaxis postnatally
  • Suture fat separately if caesarean section
  • BMI >40: 7 days postnatal heparin and TED stockings
119
Q

Describe the normal skin changes in pregnancy

A
  • Increased pigmentation (face, areolae, axillae, midline)
  • Spider naevi
  • Striae gravidarum
  • Linea nigra
  • Pruritus without rash in 20 percent of pregnancies
120
Q

Describe the effect of pregnancy on pre-existing skin disease

A

Atopic eczema

  • Worsens in pregnancy
  • Treat with emollients and bath additives
  • Hand and nipple eczema common postpartum

Acne

  • Usually improves but flares in third trimester
  • Oral/topical erythromycin can be used (NO retinoids)

Psoriasis

  • Unchanged in 40 percent, improved in another 40, worsens in 20
  • Topical steroids safe, but NO methotrexate
121
Q

Describe some specific skin diseases of pregnancy

A
  • Pemphigoid gestationis
  • Polymorphic eruption of pregnancy
  • Prurigo of pregnancy
  • Pruritic folliculitis of pregnancy

Pemphigoid gestationis

  • Rare, auto-immune, bullous disorder
  • 1:60,000
  • Late second/third trimester, lesions beginning on abdomen, spreading, sparing the face
  • Clinical diagnosis with immunofluorescence
  • Management: potent topical steroids +/- oral prednisolone
  • Associated with: preterm, SGA, recurrence in pregnancy

Polymorphic eruption of pregnancy

  • Self-limiting, auto-inflammatory disorder
  • Third trimester or immediately postpartum
  • 1:160, 75 percent of which are primigravida
  • Lower abdomen with striae, extends to thighs, buttocks, legs, arms (spares umbilicus and face)
  • Management: symptomatic, no tendency to recur

Prurigo of pregnancy

  • 1:300
  • Excoriated papules on extensor limbs, abdomen and shoulders, at 25-30 weeks
  • Higher risk in those with atopy
  • Resolves after delivery, no effects on foetus
  • Management: topical emollients and steroids

Pruritic folliculitis of pregnancy

  • Pruritic follicular eruption with papules and pustules
  • Trunk, can involve limbs
  • Similar to acne, onset at second/third trimester
  • Resolves weeks after delivery
  • Management: topical steroids
122
Q

Describe VTE in pregnancy

A

This is the cause of direct maternal death in the UK.

Pregnancy gives a hypercoagulable state, as there is an increase in factors VIII, IX, X and fibrinogen levels and a reduction in protein S and antithrombin III. There is an overall 6-10 times increase in the risk of VTE.

Risk factors (pre-existing):

  • > 35 years
  • Thrombophilia
  • Obesity
  • Previous VTE
  • Severe varicose veins
  • Smoking
  • Malignancy

Risk factors (pregnancy):

  • Multiple pregnancy
  • Pre-eclampsia
  • Multiparous
  • Caesarean section
  • Damage to pelvic veins
  • Sepsis
  • Prolonged bed rest
123
Q

How is acute VTE diagnosed?

A

Clinical diagnosis is unreliable, so accurate investigations are necessary.

Deep vein thrombosis

  • Pain in calf with varying degrees of redness/swelling
  • Compression US should be first investigation
  • Venography requires X-ray so not used unless necessary

Pulmonary embolus

  • Mild breathlessness or inspiratory chest pain
  • Sudden cardiorespiratory collapse
  • ECG, CXR and ABG
  • US lower limbs for DVT evidence
  • V/Q scan or CTPA (only if necessary)
  • D-dimer not useful as raised in pregnancy
124
Q

How is VTE managed?

A

Warfarin is contraindicated in pregnancy as it can cause limb and facial defects.

Treatment of choice is LMWHs. Women are taught to inject themselves and continue throughout pregnancy.

After delivery

  • Can change warfarin or remain on LMWH (both safe for breastfeeding)
  • NOACs not licensed in pregnancy
125
Q

How is VTE prevented prenatally?

A

Classify their risk:

High risk: antenatal MWH
- Previous VTE not related to surgery

Intermediate risk: consider antenatal LMWH

  • VTE related to surgery
  • Hospital admission
  • High risk thrombophilia
  • Medical comorbidities
  • Surgical procedure

Risk factors: 4 or more - LMWH prophylaxis from 28 weeks

  • Obesity
  • Age >35
  • Smoker
  • Varicose veins
  • Pre-eclampsia
  • Immobility
  • Family history of unprovoked VTE
  • Low-risk thrombophilia
  • Multiple pregnancy
  • ART
126
Q

How is VTE prevented postnatally?

A

Classify their risk:

High risk: 6 weeks LMWH

  • Previous VTE
  • Antenatal LMWH
  • High risk thrombophilia
  • Low risk thrombophilia + FHx

Intermediate risk: 10 days LMWH, extend if >3 factors

  • Caesarean section
  • BMI >40
  • Prolonged admission (>3 days)
  • Puerperal surgery
  • Medical comorbidities

Risk factors: 2 or more - 10 days LMWH

  • Age >3
  • BMI >3
  • Parity of >3
  • Smoker
  • Elective caesarean section
  • Family history
  • Low risk thrombophilia
  • Varicose veins
  • Systemic infection
  • Immobility
  • Pre-eclampsia
  • Multiple pregnancy
  • Preterm delivery
  • Stillbirth
  • Prolonged labour
  • PPH >1 litre or blood transfusion
127
Q

What are the prophylactic dose of LMWH?

A

20-80mg of enoxaparin depending on weight (70kg gets 40), OR,
2,500-10,000 units dalteparin depending on weight (70kg gets 5,000), OR,
3,500 - 9,000 units tinzaparin depending on weight (70kg gets 4,500)

Obstetrics (13 decks)

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