Pre-existing Maternal Disease Flashcards

1
Q

Definition of chronic hypertension (in context of pregnancy)

A

Hypertension (BP of 140mmHg systolic or higher, or 90mmHg diastolic or higher) that is present at the booking clinic, or if the woman is already taking antihypertensive medication when referred to maternity services- may be primary or secondary in origin.

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2
Q

Incidence of chronic HTN in pregnancy

A

Occurs in 0.6-2.7% of pregnancies (more common in older and obese women)- often accompanied by FHx or Hx of increased BP when taking COCP

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3
Q

Causes of chronic HTN

A
  • Primary HTN (most common-90%)
  • Secondary HTN- associated with obesity, renal disease (PKD, RAS or chronic pyelonephritis) and rarer causes including phaeochromocytoma, Cushing’s, cardiac disease
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4
Q

What phsyiological effect during pregnancy can mask HTN

A
  • The physiological fall in BP that occurs in the first trimester of pregnancy due to peripheral vasodilation
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5
Q

Complications of chronic HTN

A

Worsening HTN (heart failure, intracerebral haemorrhage), pre-eclampsia (occurs in 1 in 4), abruption, preterm delivery, LBW, requiring NICU, perinatal mortality

(Most women with pre-existing mild to moderate hypertension, with a blood pressure less than 160/110 mmHg, will have good maternal and neonatal outcomes)

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6
Q

Risk factors for developing superimposed PET

A

Renal disease, advanced maternal age, pre-existing diabetes, multiple pregnancy, BP >160/100 in early pregnancy, pre-pregnancy BMI >35, previous pre-eclampsia, antiphospholipid syndrome

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7
Q

Presentaton of previously unrecognised chronic HTN. what are the relevant investigations

A
  • HTN may worsen in late pregnancy
  • May identify fundal changes, renal bruits and radio-femoral delay
  • Proteinuria in patients with renal disease is usually noticed at booking (otherwise, should NOT have proteinuria or significant oedema

Investigations involve exclusion of secondary HTN- 24hr urinary catecholamines, renal ultrasound, U&Es, quantify proteinuria

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8
Q

Pre-pregnancy advice for women with chronic HTN

A
  • Offer women with chronic hypertension referral to a specialist in hypertensive disorders of pregnancy (maternal medicine clinic)
  • Advise women who take angiotensin-converting enzyme inhibitors (ACEis) or ARBs: That there is an increased risk of congenital abnormalities if they are used during pregnancy. To discuss alternative medications with GP etc. especially if given for management of renal disease
  • Stop antihypertensive treatment in women taking ACE inhibitors or ARBs if they become pregnant (preferably within 2 working days of notification of pregnancy)
  • Advise women who take thiazides or thiazide-like diuretics: There may be an increased risk of congenital abnormalities if taken during pregnancy. Discuss alternatives
  • Advise women who take antihypertensive treatments other than ACE inhibitors, ARBs, thiazide or thiazide-like diuretics that the limited evidence available has not shown an increased risk of congenital malformation
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9
Q

Treatment of chronic HTN in pregnancy

A

Offer advice on: weight management, exercise, healthy eating, lowering the amount of salt in their diet

Continue with existing antihypertensive treatment if safe in pregnancy, or switch to an alternative treatment, unless:
* Sustained systolic blood pressure is less than 110 mmHg
* Sustained diastolic blood pressure is less than 70 mmHg
* The woman has symptomatic hypotension

Offer antihypertensive treatment to pregnant women who have chronic hypertension and are not already on treatment if they have:
* Sustained systolic blood pressure of 140 mmHg or higher
* Sustained diastolic blood pressure of 90 mmHg or higher

Target BP should be 135/85mmHg
* Consider labetalol to treat chronic hypertension in pregnant women. Consider nifedipine for women in whom labetalol is not suitable, or methyldopa if both labetalol and nifedipine are not suitable
* Offer aspirin 75-150mg once daily for 12 weeks
* Offer placental growth factor (PlGF)-based testing to help rule out pre-eclampsia between 20 weeks and up to 35 weeks of pregnancy

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10
Q

What additional antenatal appointments should be given to women with chronic HTN

A
  • Weekly if poorly controlled
  • Every 2-4 weeks if well controlled
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11
Q

How is timing of birth affected by chronic HTN

A

Do not offer planned early birth before 37 weeks to women with chronic hypertension whose blood pressure is lower than 160/110 mmHg, with or without antihypertensive treatment, unless there are other medical indications
(In this case timing of birth should be a two-way decision between mother and obstetrician)

Thresholds for planned early birth include (usually in the context of pre-eclampsia)
* Inability to control maternal BP despite using 3 or more classes of antihypertensives in appropriate doses
* Maternal pulse oximetry less than 90%
* Progressive deterioration in liver function, renal function, haemolysis, or platelet count.
* Placental abruption
* Reverse end diastolic flow, a non-reassuring CTG

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12
Q

Intrapartum management of chronic HTN

A

During labour, measure BP hourly in women with HTN, every 15-30 mins until BP is less than 160/110

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13
Q

Antenatal foetal monitoring in women with chronic HTN

A
  • In women with chronic HTN, carry out an USS for foetal growth and amniotic fluid volume assessment, and umbilical artery doppler velocimetry at 28, 32 and 36 weeks
  • In women with chronic HTN, only carry out CTG if clinically indicated
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14
Q

Postnatal management of women with chronic HTN

A

Advise women with hypertension who wish to breastfeed that their treatment can be adapted to accommodate breastfeeding, and that the need to take antihypertensive medication does not prevent them from breastfeeding
* Antihypertensive medicines can pass into breast milk
* Most antihypertensive medicines taken while breastfeeding only lead to very low levels in breast milk, so the amounts taken in by babies are very small and would be unlikely to have any clinical effect
* Most medicines are not tested in pregnant or breastfeeding women
* Consider monitoring the BP of babies
* Offer Enalapril in the postnatal period or amlodipine for black African or Caribbean women
* If a woman has taken methyldopa to treat chronic hypertension during pregnancy, stop within 2 days after the birth and change to an alternative antihypertensive treatment
* Offer women with chronic hypertension a medical review 6–8 weeks after the birth with their GP or specialist as appropriate

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15
Q

Foetal complications associated with maternal diabetes

A
  • Congenital abnormalities are 3-4x more likely in established diabetes: Neural tube and cardiac defects, fetal lungs, related to preconceptual glucose control
  • Increased birthweight, shoulder dystocia and birth trauma, polyhydramnios due to macrosomia, 10% preterm labour
  • Foetal compromise, foetal distress and sudden foetal death are more common and related to poor control in the third trimester
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16
Q

Maternal complications associated with maternal diabetes during pregnancy

A
  • UTI, wound, and endometrial infections are more common
  • Pre-existing hypertension found in 25% of overt diabetics
  • PET more common, IHD worsens, CS or instrumental delivery more likely due to foetal compromise and foetal size. Diabetic nephropathy associated with poor foetal outcomes and retinopathy often deteriorates
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17
Q

Preconception advice for women with diabetes

A
  • If they have good glucose balance before conception and throughout their pregnancy, this will reduce the risk of miscarriage, congenital malformation, stillbirth and neonatal death
  • BUT the risk cannot be eliminated
  • The risks associated with diabetes (retinopathy, nephropathy) will increase the longer they have had diabetes
  • To use contraception until they have good glucose control
  • Agree individualised targets for self‑monitoring of blood glucose with women who have diabetes and are planning a pregnancy, taking into account the risk of hypoglycaemia
  • Advise woman to aim to keep their HbA1c level below 48mmol/mol (6.5%) if this is achievable without problematic hypoglycaemia
  • Reassure that any reduction towards this target is likely to reduce the risks of congenital malformations in the baby
  • Strongly advise women with HbA1c levels above 86 mmol/mol (10%) not to get pregnant due to the associated risks of congenital malformation etc.
  • Advise women with T1DM to aim: An FPG of 5-7mmol/L, A random plasma glucose of 4-7mmol/L
  • Blood glucose targets, glucose monitoring, medicines for treating diabetes (including insulin regimens) will need to be reviewed before and during pregnancy
  • For women with diabetes who are planning a pregnancy and who have a BMI above 27 kg/m2, offer advice on how to lose weight
  • To take folic acid (5 mg/day) until 12 weeks of gestation
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18
Q

Preconception management of women with diabetes

A
  • Offer up to monthly measurement of HbA1c levels for women with diabetes (can offer blood glucose meters) and advise more consistent monitoring
  • Offer blood ketone testing strips and a meter to women with T1DM who are planning a pregnancy, and advise them to test for ketonaemia if they become hyperglycaemic or unwell
  • Women should use metformin as an adjunct or alternative to insulin in the preconception period, when the likely benefits outweigh the potential for harm
  • STOP ALL other oral blood glucose-lowering agents before pregnancy and use insulin instead
  • Rapid-acting insulin analogues do not have adverse effects in pregnancy
  • Use isophane insulin (NPH) as the first choice for long-acting insulin during pregnancy
  • STOP ACEis and ARBs before conception and continue with alternative antihypertensives
  • Stop statins before pregnancy
  • Offer a retinal assessment and renal assessment before stopping contraception (refer to nephrologist if worrying renal function)
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19
Q

Antenatal care for women with pre-existing diabetes

A
  • Arrange contact with the joint diabetes and antenatal clinic every 1-2 weeks
  • Measure HbA1c levels at the booking appointment for all pregnant women with pre‑existing diabetes, to determine the level of risk for the pregnancy
  • Consider measuring HbA1c levels in the second and third trimesters of pregnancy DO not use routinely as a marker in second and third trimesters)
  • Level of risk rises significantly with an HbA1c level above 48 mmol/mol
  • Advise women with T1DM to test fasting, pre-meal, 1-hour post-meal and bedtime BG levels daily
  • Advise women with T2DM on multiple daily insulin injection the SAME
  • Advise women with T2DM to test their fasting and 1-hr post-meal BG only if they are managing with diet and exercise alone or taking oral therapy (or long-acting insulin)
  • Agree individualised target glucose levels
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20
Q

What should the target CPG range be for women with pre-existing diabetes

A
  • Advise pregnant women with any form of diabetes to maintain their capillary plasma glucose below:
    o FBG- 5.3 mmol/L
    o 1hr after meals- 7.7 mmol/L
    o 2hrs after meals- 6.3 mmol/L
  • All women should maintain CBG levels above 4mmol/L
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21
Q

Prevention and management of hypoglycaemia in pregnancy

A
  • Consider rapid‑acting insulin analogues (aspart and lispro) for pregnant women with diabetes
  • Advise women with insulin‑treated diabetes of the risks of hypoglycaemia and impaired awareness of hypoglycaemia in pregnancy, particularly in the first trimester
  • Advise pregnant women with insulin‑treated diabetes to always have a fast‑acting form of glucose available (e.g dextrose tablets)
  • Provide glucagon to pregnant women with T1DM, for use if needed
  • Immediately admit pregnant women with suspected diabetic ketoacidosis for level 2 critical care, where they can receive both medical and obstetric care
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22
Q

How does maternal diabetes effect the use of tocolytics

A
  • Diabetes should not be considered a contraindication to tocolysis or to antenatal corticosteroids for foetal lung maturation (should be given additional insulin)
  • Do not use betamimetic medicines for tocolysis in women with diabetes
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23
Q

Intrapartum care of women with pre-exisiting diabetes

A
  • Discuss the timing and mode of birth with pregnant women with diabetes during antenatal appointments, especially during the third trimester
  • Advise pregnant women with type 1 or type 2 diabetes and no other complications to have an elective birth IOL or C-Section, between 37 weeks and 38+6 weeks.
  • Consider elective birth before 37 weeks for women with type 1 or type 2 diabetes who have metabolic or other maternal or foetal complications
  • Diabetes should NOT be considered a contraindication to VBAC
  • Should have had an anaesthetics assessment in the third trimester
  • Monitor CBG every hour during labour and maintain CBG between 4-7mmol/L
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24
Q

How should neonates of mothers with diabetes be cared for

A
  • Babies of women with diabetes should stay with their mothers, unless there are complications or abnormal clinical signs
  • Carry out blood glucose testing routinely at 2 to 4 hours after birth in babies of women with diabetes. Should perform an ECG if there are signs of CHD or cardiomyopathy
  • Women should feed their babies: As soon as possible after birth (within 30 minutes), At frequent intervals (every 2 to 3 hours) until feeding maintains their pre‑feed capillary plasma glucose levels at a minimum of 2.0 mmol/litre.
  • Only use additional measures such as tube feeding or IV dextrose if CPG values are below 2.0mmol/L on 2 consecutive occasions or baby will not feed effectively orally
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25
Q

Postnatal care of women with diabetes

A
  • Women with insulin‑treated pre‑existing diabetes should reduce their insulin immediately after birth and monitor their blood glucose levels to find the appropriate dose
  • Explain to women with insulin‑treated pre‑existing diabetes that they are at increased risk of hypoglycaemia in the postnatal period
  • Women with pre‑existing type 2 diabetes who are breastfeeding can resume or continue metformin immediately after birth, but should avoid other oral blood glucose‑lowering therapy while breastfeeding.
  • Refer women with pre‑existing diabetes back to their routine diabetes care arrangements
26
Q

Thyroid related physiological changes in normal pregnancy

A
  • Enlargement of the thyroid gland and increased vascularisation
  • Increase in T4 and T3 and decrease in TSH in early pregnancy (Expected in early pregnancy)
  • B-HCG stimulates the TSH receptor causing an appropriate fall in TSH levels
  • TBG levels rise (due to oestrogen stimulation) causing an increase in circulating free T4
  • The low TSH and transient rise in free T4 in the first trimester-> normalised TSH and a modest decrease in T4 (within normal range) in later pregnancy
  • T4 then begins to fall with advancing gestation (controversial, but generally reported)
  • Iodine clearance is increased during pregnancy (increased intake is necessary to meet need for increased T4 production)
  • Foetal thyroxine is produced from week 12 (Dependant on mother before this point)
27
Q

Incidence of hypothyroidism in pregnancy

A

(Including subclinical hypothyroidism) occurs in 2.5% of pregnant women- symptoms can often be masked by the hypermetabolic state of pregnancy

28
Q

Causes of hypothyroidism in pregnancy

A
  • Autoimmune thyroiditis (Hashimoto’s thyroiditis) is the commonest cause in the developed world
  • Radiotherapy or surgery
  • Congenital or drug related (lithium, amiodarone)
  • Iodine deficiency
  • Infiltrative, pituitary or hypothalamic disease
29
Q

What is subclinical hypothyroidism, incidence in pregnancy

A
  • Subclinical hypothyroidism (elevated TSH, normal T4) is common but unlikely to progress to overt hypothyroidism during pregnancy (incidence: between 1.5-4%)
30
Q

Presentation of hypothyroidism in pregnancy

A
  • Often subtle and difficult to distinguish from normal symptoms of pregnancy
  • Dry skin with yellowing especially around the eyes
  • Weakness, tiredness, air loss, cold intolerance, constipation sleep disturbance
  • Goitre, delayed relaxation of deep tendon reflexes
31
Q

Preconception management of existing hypothyroidism

A
  • Check TFTs before conception if possible
  • If TFTs are not withing the euthyroid range, advise delayed conception and using contraception until the woman is stabilised on levothyroxine treatment.
  • LT4 dose should be adjusted so that pre-pregnancy TSH is lower than 2.5 mIU/L
  • Advise the woman that there is likely to be an increased demand for Levothyroxine during pregnancy and that her dose must be adjusted as soon as possible
32
Q

Antenatal management of hypothyroidism

A

Check TFTs immediately once pregnancy is confirmed and interpret results using a pregnancy-related reference range (keep TSH < 4mmol/l).
* 1st trimester: 0.1-2.5 mIU/L
* 2nd trimester 0.2-3.0 mIU/L
* 3rd trimester: 0.3-3.0 mIU/L

(urgent referral to joint obstetric and antenatal clinic)
* Check TFTs every 2-4 weeks and adjust LT4 levels accordingly
* Discuss urgently with an endocrinologist regarding initiation of, or changes to, dosage of LT4 and TFT monitoring while waiting for specialist review
* LT4 dosage should be increased at the beginning of pregnancy by 30-50%

33
Q

Postnatal management of hypothyroidism

A

TFTs should be monitored at 6-8 week postnatal check with the GP and levothyroxine should be returned to pre-pregnancy dose (breastfeeding not contraindicated)

Postpartum thyroiditis:
* Thyrotoxic phase: Propranolol (anti-thyroid drugs are avoided since likely to self resolve)
* Hypothyroid phase: thyroxine

34
Q

Complications of hypohyroidism in pregnancy

A
  • Untreated or under-treated hypothyroidism can lead to miscarriage anaemia, SGA, PET, stillbirth
35
Q

Incidence of hyperthyroidism in pregnancy

A
  • Less common than hypothyroidism, with an approximate incidence during pregnancy of 0.2%
36
Q

Causes of hyperthyroidism in pregnancy

A
  • Grave’s disease, thyrotrophin receptor activation
  • Transient gestational hyperthyroidism (associated with elevated HCG in hyperemesis gravidarum)
  • Toxic multinodular goitre or single toxic adenoma
  • Subacute thyroiditis
37
Q

Presentation of hyperthyrodism in pregnancy

A
  • Tachycardia, palpitations, heat intolerance, systolic murmur, bowel disturbance, failure to gain weight, emotional instability
  • Features of Grave’s disease: exophthalmos, tremor weight loss, pretibial myxoedema
38
Q

Complications of hyperthyroidism in pregnancy

A
  • Maternal: PIH, PET, cardiac failure, premature labour, thyroid storm
  • Foetal/ neonatal: High miscarriage rate is associated with high T4 and thyrotrophin levels, IUGR, LBW, stillbirth, thyroid dysfunction
39
Q

Preconception advice and management of pre-existing hyperthyroidism

A
  • Check TSH and FT4 levels and consider checking thyroid peroxidase antibody (TPOAb) status before conception
  • Advise any woman with untreated hyperthyroidism to delay conception and use contraception
  • If a woman has had recent radioactive iodine treatment, advise her to avoid becoming pregnant for at least 6 months
40
Q

Antenatal management of hyperthyroidism

A
  • Arrange emergency admission if the woman has a suspected serious complication such as thyrotoxic crisis, or intractable vomiting suggesting hyperemesis gravidarum
  • Arrange referral to a joint obstetric and endocrinology clinic for all women with current or previous overt or subclinical hyperthyroidism
  • Aim is to keep patient euthyroid using the lowest possible dose of antithyroid drugs necessary to maintain FT4 levels in the upper 1/3 of the normal pregnancy range
  • Dose should be adjusted every 2-4 weeks
  • Radioactive iodine therapy is contraindicated in pregnancy (destroys neonatal thyroid)
  • ONLY in 1st trimester: Propylthiouracil (crosses the placenta and in high doses may cause foetal goitre and hypothyroidism, but also considered safe in breastfeeding)
  • For the rest of pregnancy: Carbimazole.
  • Continue carbimazole/propylthiouracil at lowest acceptable doses according to TFTs
  • Safety-net regarding agranulocytosis
  • Beta blockers can additionally be used for symptomatic relief
41
Q

Postnatal management of hyperthyroidism

A

Check TFTs at 6-8 week postnatal appointment- it is recommended to continue antithyroid medication in the postnatal period

42
Q

Postnatal management of hyperthyroidism

A

Check TFTs at 6-8 week postnatal appointment- it is recommended to continue antithyroid medication in the postnatal period

43
Q

What is the incidence of asthma in pregnancy, how does pregnancy affect asthma

A

The prevalence of asthma in pregnant women is around 4-12%, making it the most common chronic condition in pregnancy. The severity of asthma during pregnancy remains unchanged, worsens or improves in equal proportions.

44
Q

What are the most common causes of asthma exacerbation in pregnancy

A
  • Respiratory viral infections are the most frequent triggers of exacerbations (34%), followed by poor adherence to inhaled corticosteroid therapy (29%)
45
Q

What are some physiological factors affecting asthma in pregnancy

A
  • Increase in free cortisol levels may protect against inflammatory triggers
  • Increase in bronchoconstricting substance (such as prostaglandins) may promote airway constriction
  • Placental gene expression of inflammatory cytokines may promote low birthweight
  • Modification of cell-mediated immunity may influence maternal response to infection and inflammation
46
Q

How can asthma affect pregnancy outcomes

A

(conflicting evidence) may be an elevated risk of:
* PIH, C-section, IUGR and LBW (all linked to poor control of asthma in pregnancy- general risk is small)

47
Q

How should asthma be managed in the intrapartum period

A
  • The same in pregnant women as in non-pregnant women and in men
  • The intensity of antenatal maternal and foetal surveillance should be based on the severity of asthma i.e the current need for therapy, symptom control, exacerbation frequency including high dose corticosteroid usage, hospitalisation and lung function (peak flow and spirometry together with risk of foetal complications)
  • Poorly controlled asthma confers an increased risk to the mother and fetus
  • Refer to maternal medicine clinic
  • Should re-educate on inhaler technique, smoking cessation etc.

Continue pre-existing asthma treatment as normal
* It is safer for women to use asthma therapy in pregnancy to achieve and maintain good control than to have uncontrolled asthma
* Inhaled corticosteroids, short or long-acting β2-agonists and theophylline do not increase the risk of maternal or neonatal outcomes such as pre-eclampsia, fetal congenital malformations, low birthweight or preterm delivery

48
Q

Intrapartum care of women with asthma

A
  • Acute, severe or life-threatening exacerbations of asthma during labour are extremely rare.
  • Women who have been on regular oral steroids may require hydrocortisone during labour.
  • LA is preferred to GA, in the case of C-section
  • Ergometrine, Syntometrine and prostaglandin may cause bronchoconstriction and should be used with caution
49
Q

Postpartum care of women with asthma

A
  • In the postpartum period there is not an increased risk of asthma exacerbations and within a few months after delivery a woman’s asthma severity typically reverts to its pre-pregnancy level
  • The same medications can be continued in the postpartum period
50
Q

Incidence of epilepsy in pregnancy

A

Epilepsy is one of the most common neurological conditions in pregnancy with a prevalence of 0.5-1%. Around 2500 infants are born to women with epilepsy (WWE) every year in the UK

51
Q

How does epilepsy effect pregnancy outcomes

A
  • The risk of death is increased ten-fold in pregnant WWE compared to those without the condition
  • Fourteen maternal deaths occurred between 2009 and 2012 attributed to SUDEP (sudden unexpected death in epilepsy)- poorly controlled seizures were the main contributing factor
  • The risk of major congenital malformation is increased in foetuses of WWE taking antiepileptic drugs. Exposure to sodium valproate and some other antiepileptics can have an adverse effect on the neurodevelopment of the newborn in the long term
  • Maternal concern over antiepileptics may lead to discontinuation or reduction in dosage taken.
52
Q

When are WWE considered low-risk in pregnancy

A

Women who have remained seizure-free for at least 10 years (With the last 5 years off antiepileptics) and those with a childhood epilepsy syndrome who are now treatment free are consider to no longer have epilepsy

53
Q

Common types of seizure in epilepsy and their impact on foetus/ pregnancy

A

Tonic-clonic seizures:
* Dramatic events with stiffening, then bilateral jerking and a post seizure state of confusion and sleepiness
* Associated with a variable period of foetal hypoxia- highest association with SUDEP

Absence seizures:
* Generalised seizures that consist of brief blank spells associated with unresponsiveness, which are followed by rapid recovery
* Effects mediated through brief loss of awareness although physiological effects are modest- worsening absence seizures predispose to tonic-clonic seizures

Myoclonic seizures:
* Short jerking (myoclonic jerks) are a key feature (often precedes a tonic-clonic convulsion)
* Occurs more frequently after sleep deprivation and in the period soon after waking or when tired- may lead to falls which pose a risk to pregnancy

Focal seizures:
* Symptoms are dependant on the region of the brain affected- may undergo secondary generalisation
* Also poses a risk of variable hypoxia and SUDEP

54
Q

Differentials for epilepsy in pregnancy

A
  • In pregnant women presenting with seizures in the second half of pregnancy, which cannot be clearly attributed to epilepsy, immediate treatment should follow protocols for eclampsia until definitive diagnosis is made through neurological assessment
  • Other causes: cerebral venous sinus thrombosis, space-occupying lesions, reversible cerebral vasoconstriction syndrome, vasovagal syncope, metabolic (hypoglycaemia, hyponatraemia, Addisonian crisis), arrythmia, dissociative seizures (‘non-epileptic attack disorder’
55
Q

Preconception management and advice for WWE

A
  • WWE should be reassured that most mothers have normal babies and that the risk of congenital malformations is low if they are not exposed to antiepileptics in the periconception period (Risk is similar to the background risk for the general population)
  • The risk of congenital abnormalities in the foetus is dependant on the type, number and dose of antiepileptics
  • Lamotrigine, and carbamazepine monotherapy at lower doses have the least risk of major congenital malformation in the offspring

The most common major congenital malformations associated with antiepileptics are neural tube defects, congenital heart disorders, urinary tract disorder and cleft palate
* Sodium valproate-> neural tube defects, fascial cleft, hypospadias
* Phenobarbital/ phenytoin-> cardiac malformations
* Carbamazepine-> cleft palate
* Women should be informed about the long-term adverse impact on neurodevelopment of the newborn following exposure to sodium valproate (In utero exposure to carbamazepine and lamotrigine does not appear to influence neurodevelopment)
* All WWE should be advised to take 5 mg/day folic acid prior to conception and to continue intake until at least the end of the first trimester to reduce risk of malformations
* The lowest effective dose of the most appropriate antiepileptic should be used and exposure to sodium valproate and POLYTHERAPY should be avoided
* Two-thirds of WWE will not have seizure deterioration in pregnancy (67% do not experience a seizure)

Women who have had a seizure in the year prior to conception require closer monitoring during pregnancy

56
Q

Preconception management and advice for WWE

A
  • WWE should be reassured that most mothers have normal babies and that the risk of congenital malformations is low if they are not exposed to antiepileptics in the periconception period (Risk is similar to the background risk for the general population)
  • The risk of congenital abnormalities in the foetus is dependant on the type, number and dose of antiepileptics
  • Lamotrigine, and carbamazepine monotherapy at lower doses have the least risk of major congenital malformation in the offspring

The most common major congenital malformations associated with antiepileptics are neural tube defects, congenital heart disorders, urinary tract disorder and cleft palate
* Sodium valproate-> neural tube defects, fascial cleft, hypospadias
* Phenobarbital/ phenytoin-> cardiac malformations
* Carbamazepine-> cleft palate
* Women should be informed about the long-term adverse impact on neurodevelopment of the newborn following exposure to sodium valproate (In utero exposure to carbamazepine and lamotrigine does not appear to influence neurodevelopment)
* All WWE should be advised to take 5 mg/day folic acid prior to conception and to continue intake until at least the end of the first trimester to reduce risk of malformations
* The lowest effective dose of the most appropriate antiepileptic should be used and exposure to sodium valproate and POLYTHERAPY should be avoided
* Two-thirds of WWE will not have seizure deterioration in pregnancy (67% do not experience a seizure)

Women who have had a seizure in the year prior to conception require closer monitoring during pregnancy

57
Q

Antenatal care for WWE

A
  • Pregnant WWE should have access to regular planned antenatal care with a designated epilepsy care team
  • Women who become unexpectedly pregnant should be urgently referred- it is never recommended to stop or change antiepileptics without a prior discussion. Even high-risk drugs like sodium valproate are still the drugs of choice for certain epilepsies and a discussion of risks and benefits is mandatory
  • Early pregnancy can be an opportunity to screen for structural abnormalities. The foetal anomaly scan at 18+0–20+6 weeks of can identify major cardiac defects in addition to neural tube defects.
  • All WWE should be offered a detailed ultrasound
  • Biochemical screening with maternal serum alphafetoprotein when combined with ultrasonography increases the detection rate for neural tube defects to 94–100%
  • In the antenatal period women should be regularly assessed for RFs for seizures: sleep deprivation and stress, adherence to AEDs, seizure type and severity
  • All babies born to WWE taking enzyme-inducing AEDs (carbamazepine, phenytoin phenobarbital) should be offered 1mg IM Vitamin K
58
Q

What are some obstetric risks associated with AED use in WWEs

A

o In WWE in general: Spontaneous miscarriage, antepartum haemorrhage, hypertensive disorders, IOL, C-section, preterm delivery, FGR, PPH
o There is no increased risk of perinatal death
o In WWE taking AEDs: IOL, FGR, PPH, NICU

59
Q

Intrapartum care of WWE

A
  • WWE should be reassured that most will have an uncomplicated labour and delivery
  • The diagnosis of epilepsy per se is not an indication for planned caesarean section or induction of labour
  • Pregnant WWE should be counselled that the risk of seizures in labour is low. Tonic clonic seizures occur in around 1-2% of WWE in labour and in a further 1-2% within 24 hours of delivery
  • Adequate analgesia and appropriate care in labour should be provided to minimise risk factors for seizures such as insomnia, stress and dehydration.
  • Long-acting benzodiazepines such as clobazam can be considered if there is a very high risk of seizures in the peripartum period
  • AED intake should be continued during labour. If this cannot be tolerated orally, a parenteral alternative should be administered.
  • Seizures in labour should be terminated as soon as possible to avoid maternal and fetal hypoxia and foetal acidosis. Benzodiazepines are the drugs of choice. Left lateral tilt should be established alongside maintenance of airway and oxygenation at all times
  • In those with intravenous access, lorazepam given as an intravenous dose of 0.1 mg/kg (usually a 4 mg bolus, with a further dose after 10−20 minutes)
  • IF there is no IV access, diazepam 10-20mg rectally can be given
  • Continuous foetal monitoring is recommended in women at high risk of a seizure in labour, and following an intrapartum seizure
60
Q

Postnatal care for WWE

A
  • Although the overall chance of seizures during and immediately after delivery is low, it is relatively higher than during pregnancy.
  • Continue their AEDs postnatally.
  • Mothers should be well supported in the postnatal period to ensure that triggers of seizure deterioration such as sleep deprivation, stress and pain are minimised
  • If the AED dose was increased in pregnancy, it should be reviewed within 10 days of delivery to avoid postpartum toxicity
  • Based on current evidence, mothers should be informed that the risk of adverse cognitive outcomes is not increased in children exposed to AEDs through breast milk- should be encouraged to breastfeed