Chapter 5 - Medical disorders in pregnancy Flashcards

1
Q

“will my epilepsy get worse during pregnancy?”

A

37% of womens seizures increase
13% decrease
50% remain the same

**those who’s epilepsy is poorly controlled are at highest risk of increasing seizure frequency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

“Will my seizures affect my baby?”

A
  • Usually fetuses tolerate seizures without complications, but status epilepticus increases the risk of demise
  • However, women with epilepsy have an increased risk of congenital anomalies (mostly due to meds, especially polypharmacy but even in women off meds. Higher dose = increased risk. Dividing doses may reduce peak = reduce risk.
  • Change before becoming pregnant, once pregnant don’t change doses as risk has already occured + increase risk of poor control.
  • Taking folic acid can help to minimize risks
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the risks of anticonvulsants during pregnancy?

A

• Teratogenicity: congenital anomalies or fetal anticonvulsant
syndrome.
• Neonatal withdrawal.
• Vitamin K deficiency (enzyme inducers) –> haemorrhagic disease of
newborn.
• Developmental delay and behavioural problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Differentials for a woman with her first seizure in pregnancy

A
• Eclampsia.
• Epilepsy.
• Infection:
- meningitis
- encephalitis
- abscess.
• Metabolic:
- drug or alcohol withdrawal
- drug toxicity
- hypoglycaemia
- electrolyte imbalance (raised Na/ca, decreased Na).
• Severe hypoxia.
• Space-occupying lesion.
• Vascular:
- cerebral vein thrombosis
- thrombotic thrombocytopaenic purpura (TTP)
- cerebral infarction or haemorrhage.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Inx for a woman with her first seizure in pregnancy

A
  • CT or MRI (preferable) + Neuro review
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Risks of valproate to fetus

A
  • Neural tube defects: increase 10-fold (1–2%).
  • Genitourinary anomalies (hypospadias).
  • Cardiac anomalies.
  • Facial clefts.
  • Neurodevelopmental delay: increase 3.5-fold.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Risks of carbamazepine to fetus

A
  • Neural tube defects (0.5–1%).
  • Cardiac anomalies.
  • Facial clefts.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Risks of phenytoin to fetus

A
  • Facial clefts: i 5-fold.

* Cardiac anomalies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pre-pregnancy management of epilepsy

A

1) confirm epilepsy
2) Educate
3) use least amount of meds
4) Consider stopping if seizure free for 2years
5) 5mg folic acid for 12weeks before conception + continue until delivery
6) 4% risk of child with epilepsy if one parent affected, 15% if both affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Antenatal management of epilepsy

A

1) Don’t change meds
2) Prenatal screening (a-fetoprotein for neural defects + anomaly scan for clefts and cardiac abnormalities)
3) Fetal echo at 22 weeks
4) Vit K 10mg/day for last 4 weeks of pregnancy (neonatal coagulopathy)
5) General advice - showers not bathes ect. good amount of sleep
6) some women have to go up on meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

labour in epileptics

A
  • Aim vaginal
  • Labour increases risk of seizures
  • control seizures with benzos
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Post-natal care for epileptics

A

• Neonatal vitamin K to lower risk of haemorrhagic disease of the newborn.
• Breast-feeding is not contraindicated (anti-convulsants reach breast milk and thus slow withdrawal occurs, although phenobarbital and benzodiazepines may cause sedation in the baby).
• If the anticonvulsant dose was increased reduce it back slowly
• Contraception with enzyme-inducing drugs:
- COCP containing 50 micrograms oestrogen with a shorter pill-free interval
- progestogen-only pill (POP) is less effective
- intrauterine contraceptive device (IUCD) is ideal.
• General advice (bathing and feeding) to minimize risk of harm to baby from seizures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When during pregnancy is there an increased risk of CVA?

A

Post-partum - There is a 9-fold increased risk for infarcts and 28-fold increase for haemorrhagic stroke in the first 6wks postpartum
compared with non-pregnant women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Symptoms of CVA

A
  • Abrupt onset of weakness.
  • Sensory loss.
  • Dysphasia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

RF for CVA

A
  • Smoking.
  • Diabetes.
  • Hypertension.
  • Hypercholesterolaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

The most common cause of SAH outside pregnancy

A

Ruptured berry aneurysm,
but arteriovenous malformations (AVMs) may dilate in pregnancy due to
the effect of oestrogen, resulting in a similar incidence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Presentation of SAH

A
  • Headache.
  • Vomiting.
  • Loss of or impaired consciousness.
  • Neck stiffness.
  • Focal neurological signs.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Mx of SAH

A

• Early treatment = reduce the chance of subsequent
bleeding (the risk is high for AVM).
• Surgery; excision of the AVM, coiling, or clipping.
• Interventional radiology is associated with exposure of the fetus to large doses of radiation.
• Nimodipine to decrease vasospasm.
• Delivery:
- labour is high-risk for bleeding, recommend elective CS if the lesion is inoperable
• epidural anaesthesia is contraindicated with a recent subarachnoid haemorrhage (SAH) due to raised intracranial pressure
• if the lesion has been successfully treated = vaginal delivery (a longer passive 2nd stage with early use of assisted delivery may reduce the risk of rebleeding).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of CVAs in pregnancy

A
Infarcts
• Pre-eclampsia/eclampsia.
• Central nervous system (CNS) vasculitis.
• Carotid artery dissection.
• Emboli:
- itral stenosis
- peripartum cardiomyopathy
- endocarditis
- paradoxical emboli.
• Coagulopathies:
- Thrombophilia
- Antiphospholipid syndrome.
-Thrombotic thrombocytopaenic purpura.
- Cerebral vein thrombosis.
Haemorrhagic
• Pre-eclampsia/eclampsia.
• DIC.
• AVM.
• Ruptured berry aneurysm.
• CNS vasculitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Inx of CVA

A
**Liaise with neuro
• M RI or CT scan of head.
• Cerebral angiography +/– venography.
• Echocardiogram.
• Carotid Dopplers.
• Thrombophilia screen and antiphospholipid antibodies.
• Homocystine level/methylenetetrahydrofolate reductase (MTHFR)
screen .
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Antenatal mx of cardiac disease

A

1) MDT mx
2) Optimize CV stability - ?surgery, optimize meds
3) Educate on risks
4) Estimate CV tolerability - NYHA exercise tolerance, pulmonary Ht or cyanosis
5) Consider if termination is necessary
6) Correct factors that may cause decompensation - anaemia, infection, Htn or arrhythmia
7) Monitor with maternal echos and fetal growth US (IUGR or death in utero especially with cyanosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Should all women with CV disease have a CS?

A
  • Aim for vaginal delivery with a short 2nd stage unless; aortic root >4.5cm, LVEF <30%, aortic dissection or aneurysm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Key points in mx of women CV during labour

A

1) Have a clear pre-set plan
2) Consider whether CS or vaginal delivery is necessary
3) Aim for a short second phase
4) Monitoring throughout
5) Minimize blood loss by active mx of 3rd stage + oxytocin infusion (avoid ergometrine and prostaglandins)
6) Epidurals may help CV stability (controlling HR + BP due to pain)
7) Strict fluid mx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Describe 5 normal haemodynamic changes in normal pregnancy

A

1) Peripheral vasodilation –> lowers BP
2) CO increases during pregnancy and further during labour
3) CO increases further following delivery due to increased venous return
4) Colloid osmotic pressure falls –> increased risk of pulmonary oedema
5) Hypercoagulability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Does CO increase or decrease after delivery?

A

CO increases following delivery due to increased venous return:
• relief of vena caval obstruction
• tonic uterine contraction (expels blood into systemic circulation).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which groups of women with CV disease are considered as high risk aka 50% mortality?

A
  • Pulmonary hypertension.
  • Aortic dissection.
  • Complicated aortic coarctation.
  • Marfan’s syndrome with significant aortic root involvement.
  • Myocardial infarction.

Moderate risk
• Mitral stenosis NYHA class 3 or 4.
• Severe aortic stenosis.
• Mechanical heart valves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Risk of artifical heart valves in pregnancy

A
  • Women have near normal cardiac function
  • Risk is due to anti-coagulants
  • But they must be continued due to risk of stoke and valve thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Benefits and risks of LMWH

A
  • Less maternal bleeding
  • No risk to fetus as it doesn’t cross the placenta
  • Increased risk of embolic events, valve thrombosis, osteoporosis and heparin induced thrombocyopenia than warfarin

= safer for the baby, less safe for the mum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Benefits and risks of warfarin

A
  • Increased risk of miscarriage, warfarin embryopathy, maternal and neonatal bleeding
  • long half life
  • Lower risk of embolic events and valve thrombosis than LMWH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

By what time should all women on warfarin be switched to LMWH?

A

37weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When should LMWH be stopped and restarted?

A

stopped in labour, restarted after delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Can warfarin be restarted after delivery?

A

No, restart 7-10 days after

33
Q

Reversal agent of warfarin

A

FFP, vit k, prothrombin complex concentrates

34
Q

Reversal agent of LMWH

A

Protamine sulphate

35
Q

Which anticoagulant can be given to breast feeding mothers?

A

Both heparin and LMWH is safe

36
Q

What should be added to LMWH in women with artificial valves?

A

Low dose Aspirin

37
Q

Are anticoagulants required for bio-prosthetic valves?

A

No, unless AF or arrhythmia

38
Q

In which patients should endocarditis prophylaxis be given?

A

High risk
• Prosthetic heart valves (mechanical or tissue).
• Previous bacterial endocarditis.
• Complex cyanotic heart disease (Fallot’s tetralogy, transposition).
• Surgically constructed systemic/pulmonary shunts.

Moderate risk
• Hypertrophic cardiomyopathy.
• Acquired valvular lesions.
• Mitral valve prolapse with severe regurgitation.
• Other congenital cardiac malformations.

39
Q

What can be given as endocarditis prophylaxis?

A

• Amoxicillin 1g IV + gentamicin 120mg IV at onset of labour or
rupture of membranes, then amoxicillin 500mg orally 6h later.

• Vancomycin 1g IV or teicoplanin 400mg IV if penicillin allergy with
gentamicin 120mg IV.

40
Q

What is the most common lesion caused by rheumatic heart disease?

A

Mitral stenosis

41
Q

Consequences of mitral stenosis in pregnancy

A

1) Pulmonary oedema (greatest in labour) –> Mx Diuretics +/- BB (for increased HR)
2) Thromboembolism

42
Q

Risks of mitral regurg in pregnancy

A

Mitral regurgitation is well tolerated in pregnancy; heart failure and endocarditis are rare.

43
Q

Mortality of MI in pregnancy

A

20% immediate, 32% overall

44
Q

Atypical symptoms of MI in pregnancy

A

Abdo pain, vomiting and dizziness

45
Q

Does a single ECG in a pain free patient rule out MI?

A

No, consider serial ECG

46
Q

Mx of MI

A
  • Mx at coronary care unit
  • PCI first choice
  • Thrombolysis has a high rate of fetal loss but consider if PCI not possible
  • Aim for delivery vaginally
  • If previous Hx of MI - give aspirin throughout pregnancy
47
Q

Give the diagnosis + Mx:

• Presentation: breathlessness, palpitations, oedema, poor exercise
tolerance, and embolic phenomena.
• Echo: global dilatation of all four chambers of the heart

A

Cardiomyopathy/paripartum cardiomyopathy

Management: supportive; should include angiotensin-converting
enzyme inhibitors (ACEIs) and anticoagulation
  • Deliver if diagnosed antenatally
  • Consider heart transplant if failure despite meds
  • Recurrence risk is high
48
Q

Main risk of marfans in pregnancy

A

Aortic dissection + rupture

  • Manage Htn with BB
49
Q

Describe the physiology of Hb during pregnancy

A
  • Plasma volume expands by up to 50%, greater than the expansion of red cell mass –> dilution with a drop in Hb

**Anemia = Hb <10.5 in pregnancy

**Pregnancy has a 2-3x increase in iron requirement + 10-20x increase in folate requirement

50
Q

Commonest cause of anaemia in pregnancy

A

IDA (90%)

51
Q

Tx of IDA in pregnancy

A

Oral iron + Vit C promotion (orange juice), don’t take with tea

  • Expect an improvement of 1 Hb per day, if not consider IV
  • Transfusion threshold <70
52
Q

RF for folate deficiency

A
  • poor nutritional status
  • haematological problems with a rapid turnover of blood cells, e.g. haemolytic anaemia and haemoglobinopathies
  • drug interaction with folate metabolism, e.g. antiepileptics.
53
Q

Dx of folate deficiency

A

Raised MCV, Low serum and red cell folate

54
Q

Those at high risk of neural tube defect

A
  • On anticonvulsants
  • with a previous child affected with a neural tube defect
  • folate deficiency
  • with diabetes
  • with a BMI >35
  • with sickle cell disease.
55
Q

Tx for women at high risk of neural tube defects

A

5mg/daily

56
Q

Folic acid dose for women not at high risk of neural tube defects

A

400mcg/day

57
Q

RF B12 deficiency

A

Pernicious anaemia, terminal ileum disease, and strict vegans.

  • continue tx throughout pregnancy
58
Q

Risks of sickle cell in pregnancy

A
  • Crises are more common during pregnancy.
  • increased Risk of pre-eclampsia.
  • increased Risk of delivery by CS s to fetal distress.
59
Q

Clinical features of sickle cell disease

A

• Haemolytic anaemia.
• Painful crises.
• Hyposplenism (chronic damage to the spleen results in atrophy).
• Increased risk of infection (UTI, pyelonephritis, pneumonia,
puerperal sepsis).
• Avascular necrosis of bone.
• Increased risk of thromboembolic disease (pulmonary embolism
(PE), stroke).
• Acute chest syndrome (fever, chest pain, tachypnoea, increased WCC,
pulmonary infiltrates).
• Iron overload: leads to cardiomyopathy.
• Maternal mortality 2%.

60
Q

Mx of sickle cell anaemia

A
  • MDT with hematologist
  • Prepregnancy counselling - screening the partner for carrier status (PGD)
  • Stop iron chelating before pregnancy
  • Echo if iron overload
  • 5mg/day folic acid + penicillin for hyposplenism
  • Monitor Hb and HbS
  • Screen for urine infections
  • Tx crisis’ with analgesia, O2, rehydration and Abx if infection
  • Reg assessment of fetal growth
  • Aim vaginal delivery
  • Consider antenatal and postnatal thromboprophylaxis
61
Q

Fetal risks of maternal sickle cell disease

A

• IUGR.
• Prematurity.
• Stillbirth.
**Perinatal mortality is increased 4–6-fold

62
Q

Consequences of Hb Barts

A

Four defective alpha genes, incompatible with life —> hydrops + premature + severe early onset pre-eclampsia

Aka Alpha Thalassaemia major

63
Q

Cause + consequence of HbH

A

3 defective alpha genes leading to chronic haemolysis and iron overload

64
Q

Consequences of thalassaemia trait in pregnancy

A

Usually asymptomatic but may become anaemic in pregnancy

65
Q

Is beta thalassaemia major fatal like alpha?

A

No but women are often transfusion dependent with iron overload, delayed puberty and subfertility

**repeated transfusions leads to endocrine dysfunction

66
Q

Mx of pregnancy with thalassaemia

A
  • check ferritin - replace with oral iron if low
  • folic acid 5mg daily
  • IM folate if not responding to oral folate
  • avoid IV iron
  • transfuse if necessary
  • genetic counselling
  • PGD
67
Q

Which groups of women are screened for thalassaemia during pregnancy?

A

Women who are from the med, Middle East, india, Asia, Africa or West Indies by origin have electrophoresis at booking

68
Q

FBC reveals low mcv and low Mchc, what should be investigated

A

Alpha thalassaemia

Also if microcytic anaemia with normal MCHC, in IDA MCHC is also low

69
Q

How does haemophilia affect women?

A

Female carriers do not usually have bleeding issues but clotting factors are often 1/2 of normal

  • There is increased risk of post-partum haemorrhage (factor VIII, but not factor IX, increases in pregnancy in normal women and
    haemophilia carriers. Therefore, women with factor IX deficiency are
    most at risk while pregnant)
70
Q

Does ITP affect the fetus?

A

Yes, as IgG antiplatelet antibodies can cross the placenta and cause fetal thrombocytopenia

71
Q

Mx of ITP in pregnancy

A
  • FBC every 2 weeks
  • Bleeding unlikely if plt >50
  • If plt <50 start oral steroids or IV immunoglobulin if failure to respond
72
Q

Causes of thrombocytopaenia in pregnancy

A
  • Spurious.
  • Gestational thrombocytopaenia.
  • Pre-eclampsia.
  • Idiopathic thrombocytopaenic purpura.
  • Thrombotic thrombocytopaenic purpura.
  • Disseminated intravascular coagulopathy.
  • Systemic lupus erythematosus.
  • Bone marrow suppression.
73
Q

Effects of pregnancy on asthma

A

1/3 no change, 1/3 improvement, 1/3 deteriorate

74
Q

Effect of asthma on pregnancy

A

No effect, minor association with low birth weight and pre-term labour

75
Q

Can Mx of asthma be continued during pregnancy?

A

Yes, treatment safe even morphine sulfate

LT steroids risk addisonian crisis during labour (tx with hydrocortisone)

Safe to breast feed

76
Q

Tx of acute asthma

A
  • nebulized bronchodilators
  • IV steroids
  • nebulized ipratropium
  • IV aminophylline or IV salbutamol
    • /– antibiotics if evidence of infection.
77
Q

Affects of CF on fertility

A
  • Lower life expectancy (41)
  • Most men are infertile due to congenital absence of vas deferens
  • Women are subfertile due to unfavourable mucus, reduced BMI and anovulation
78
Q

Tx of pneumonia in pregnancy

A

Amoxicillin at a higher dose e.g. 500mg TDS due to increased renal clearance

79
Q

Effect of inflammatory bowel disease on pregnancy

A

• Fertility, miscarriage, stillbirth, and fetal anomaly rates are not affected
in women with quiescent or well-controlled disease.
• Active disease at conception, first presentation in pregnancy, colonic rather than small bowel disease alone, active disease after resection,
and severe disease treated by surgery are all associated with increased
risk of miscarriage, stillbirth, prematurity, and low birth weight.