A 25-year-old pregnant woman at 32 weeks gestation presented with palpitations and sweating for 1 week and was found to have an enlarged thyroid gland, increased thyroid hormones, and positive thyroid antibodies, consistent with Graves' disease developing during her pregnancy. Her mother also had a history of thyroid problems. She was diagnosed with hyperthyroidism in pregnancy likely due to Graves' disease and started on antithyroid medication to control her thyroid function and protect the health of her pregnancy.
2. Case scenario
A 25 years old, G3P2 @32 weeks complains of having palpitations for 1 week.
symptoms was associated with heat intolerance with sweating more than
normal.Upon further questioning , patientâs mother had history of thyroidectomy.
On examination,
BP : 138/88
PR : 120bpm
T : 37.6
Per-abdomen
uterus @ 32 weeks size
s/c
head â
EFW: 2.4-2.6kg
FHR : 141bpm
3. diffuse painless symetrically enlarged thyroid swelling seen over
the anterior neck
Lungs : clear, CVS : no murmur
bloods taken , noted TSH reduced, T3 & T4 increased with TrAB
positive
USG : enlarged thyroid gland with increased echogenticity
4. Physiological Changes in Pregnancy
âTotal T4 â and Total T3 â > 50% compared to normal women
âDaily iodine requirement > 50% compared to normal woman
âPregnancy is a state of relative iodine deficiency
TSH (mU/L) fT4 (pmol/L) fT3 (pmol/L)
Non-pregnant 0.3 â 4.2 12 â 22 3.1 â 6.8
1st Trimester 0 â 4.5 10 â 16 3 â 7
2nd Trimester 0.5 â 5.5 9 â 15.5 3 â 5.5
3rd Trimester 0.5 â 4 8 â 14.5 2.5 â 5.5
5. Hyperthyroidism
âOccurs in 1 in 500 pregnancies, over 50% have a family hx of
autoimmune thyroid disease
ââ95% are due to Graveâs disease
âOther causes: gestational transient thyrotoxicosis, thyroiditis, toxic
nodule
Clinical features
âSymptoms may overlap with normal pregnancy
âHeat intolerance, palpitations, vomiting, tachycardia, goitre, emotional lability
âMost discriminatory features â weight loss, persistent tachycardia, tremor, lid
lag, exophthalmos
9. Antenatal care
âAntithyroid drugs (ATDs)
âMost commonly used are carbimazole (CMZ) and propylthiouracil (PTU)
âOnset up to 3-4 weeks
âBoth cross the placenta (PTU less than CMZ)
âHigh doses may cause fetal hypothyroidism and goitre, but unlikely if PTU
â¤150mg/day or CMZ â¤15mg/day
âIncreased risk of teratogenicity for both ATDs (CMZ > PTU)
â Aplasia cutis, abdominal wall defects, atresia of digestive tract, urinary tract, choanal
atresia, ventricular septum defect
âPTU has rare side effect of liver impairment (1 in 10,000)
10. Treatment for newly diagnosed
1st trimester Initial dose: PTU 150-400mg for 4-6 weeks
Usual maintenance dose: 50-150mg
2nd and 3rd trimester Initial dose: CMZ 15-40mg for 4-6 weeks
Usual maintenance dose: 5-15mg
⢠Newly diagnosed
⢠If already on CMZ maintenance
⢠Continue at its lowest dose that maintain clinically euthyroid
⢠No need to switch, although PTU preferably in 1st trimester
11. âBeta blocker (propranolol, metoprolol)
âTo improve sympathetic symptoms (tachycardia, sweating, tremor)
âDiscontinue once anti-thyroid drugs take effect / clinically improved (â 3weeks)
âRAI
âContraindicated in pregnancy and breastfeeding mothers
âSurgery
âIndications: dysphagia, stridor, suspected Ca, allergic to ATDs
âCan be safely performed in 2nd trimester
âEnsure euthyroid prior to surgery
âRequire replacement post surgery
12. âMonitoring
âRefer combined clinic for multidisciplinary management
âMonitor TFT monthly for newly diagnosed
âMonitor TFT 4-6 weekly if any adjustment of medication
âAim T4 at upper limit of normal with lowest dose of ATDs.
âCounsel patient to report any signs of infection, sore throat, fever, jaundice
â Send FBC, stop CMZ if neutropenia
âFetal surveillance
âSerial scan for growth
âFetal heart rate (rare but dangerous risk of fetal thyrotoxicosis)
âFetal neck (look for goitre)
13. Intrapartum
âLabour and delivery may precipitate thyroid storm
Post-partum
âSend cord blood for TFT
âRefer paeds for possibility of neonatal thyrotoxicosis / hypothyroidism
âEncourage breastfeeding, generally safe especially with low maintenance dose
âAvoid RAI during breastfeeding
âContraception
âBe aware of Graveâs disease flare, especially if medication was reduced during
pregnancy â continue follow up
16. Pre-Pregnancy care
⢠Multidisciplinary
care.
⢠Optimize
thyroxine doses
pre-pregnancy.
⢠Advise delay
pregnancy until
achieve good
control.
Antenatal care
⢠Refer next slide
Intrapartum care
⢠Generally similar
to normal
pregnancy.
Post-partum care
⢠Ensure cord
blood taken for
TFTs.
⢠Observe for
postpartum
depression
(commoner in
patients with
thyroid
antibodies).
⢠Follow-up at
physician clinic.
MANAGEMENT
17. Management: Antenatal Care
⢠Thyroxine replacement therapy:
⎠Usual maintenance dose of 100 - 200 ug/day.
⎠Reassure patient on safety of maternal therapy.
⢠Newly diagnosed patient:
⎠Begin thyroxine replacement immediately - 100 ug/day is appropriate.
⢠If patient already on treatment:
⎠Continue thyroxine, check TFTs in early pregnancy to ensure adequate therapy.
⎠Isolated raised TSH in 1st trimester is common, does not need to increase thyroxine dose unless confirmed with low fT4 or raised
TSH (>4mU/L) despite normal fT4.
⢠Patient monitoring:
⎠Refer Combined Clinic for multidisciplinary management.
⎠Following any adjustments to thyroxine dose, check TFTs every 4 - 6 weeks.
⎠In stable euthyroid patients, can be done less frequently every 2-3 months or at least every trimester.
⢠Fetal surveillance:
⎠Serial scans for growth and goitre, especially if newly diagnosed or undertreated hypothyroidism.
18. Subclinical Hypothyroidism
⢠Definition: Serum TSH above normal range and fT4 within normal
range in an asymptomatic patient.
⢠Currently, insufficient evidence to support
⎠routine T4 treatment
⎠target TSH of <2.5 mU/L
⢠BUT, if thyroid antibody positive:
⎠Do TFT's before pregnancy.
⪠If rising TSH or reduced free T4: Commence thyroxine treatment.
⪠TSH 2.5 - 4.0 mU/L does not require treatment.
⎠In pregnancy, consider treatment with 25 - 50 ug thyroxine.
19. Contraception
-estrogen or both estrogen and progesterone can alter that delicate balance of free and bound thyroid
hormone in your body.
-The estrogen in birth control pills increases the amount of thyroid binding proteins available to bind to thyroid
hormone. What does this mean for you? If you have more thyroid hormone bound to proteins, youâll have less
free T4 in your body thatâs able to do its job.
-Progesterone and thyroid hormones have a reciprocal relationship. You need adequate amounts of thyroid
hormone for your ovaries to make progestrone but progesterone also helps the thyroid. For example, research
shows that progesterone can increase thyroid hormone levels in the blood. Progesterone also decreases the
amount of protein that carries thyroid in the blood so that more thyroid hormone can be free and get into the
cells.
21. The approach to diagnosis of asthma during pregnancy is the same as to any
non-pregnant asthma patient.
22. ď The management of asthma in pregnant patients is the same as for non-
pregnant patients, with Inhaled corticosteroids(ICS) being the preferred
long-term controller medication.
ď The following should be emphasised:
⢠patient education on good asthma control
⢠frequent monitoring (4 - 6 weeks)
⢠maintenance, reliever and anti-leukotriene should be continued
⢠stepping down medication should be done after delivery if asthma is well
controlled
24. Management: Pre-Pregnancy Care
Optimise patient's asthmatic control - check her inhaler's technique.
Counsel on:
ďź Importance and safety of continuing asthma treatment.
ďź Risk of adverse maternal and fetal outcomes with poorly controlled asthma:
⢠Maternal - those with severe asthma are at greater risk of deterioration (e.g.
life-threatening AEBA); some association with PIH/PE.
⢠Fetal - Low birth weight, preterm birth, FGR, neonatal morbidity.
⢠Reassure that if asthma is well-controlled throughout pregnancy, little or no
increased risk of poor outcome.
ďź If smokes - advice to stop smoking.
ďź Avoidance of asthma triggers.
ďź Indications for an increase in inhaled steroid dosage.
25. Management: Antenatal Care
⢠Emphasis in management is on prevention, rather than the treatment of acute attacks.
⢠Good control: Follow-up at local clinics by MO/FMS
⢠Poorly controlled: Refer to Chest Clinic for optimisation of therapy.
⢠Management is the same as in the non-pregnant patients.
⢠Medications use in asthma and pregnancy:
ďź Reassure that all the drugs appear to be safe in pregnancy and lactation.
ďź B2-agonists (short and long acting) is safe in pregnancy.
ďź Corticosteroids (inhaled and oral) is safe in pregnancy.
⢠If patients on oral steroids: Monitor BP, screen for GDM, if diabetic â monitor glycaemic
control closely.
⢠Fetal monitoring: Serial growth scans especially in poorly controlled asthmatic patients.
26. STEP 1 Low-dose inhaled corticosteroid (e.g.: Beclomethasone or Budesonide 200 mcg BD)
STEP 2 Low-dose inhaled corticosteroid and inhaled long-acting B2 agonist
(LABA) (e.g.: Salmeterol or Formoterol)
Combination inhalers â
Symbicort (Budesonide with Formoterol)
Seretide (Fluticasone with Salmeterol)
STEP 3 If no response, start medium-dose inhaled corticosteroid (eg: Beclomethasone or Budesonide
400 mcg BD) plus inhaled LABA
If response remains inadequate consider:
Theophylline
Leukotriene receptor antagonist (Montelukast)
Inhaled long acting antimuscarinic (Tiotropium)
STEP 4 Consider trials of:
⢠High dose inhaled corticosteroids (Beclomethasone or Budesonide up to 1000 mcg BD) and
inhaled LABA
⢠Theophylline
⢠Leukotriene receptor antagonist
⢠Oral B2-agonist (Salbutamol)
⢠Inhaled long- acting antimuscarinic
STEP 5 Long-term oral corticosteroids at lowest possible dose
Maintain high-dose inhaled corticosteroid
Consider steroid-sparing agent
Recommended Management of Asthma in Pregnancy
27. Management: Intrapartum Care
⢠Continue inhalers.
⢠If patients on oral steroids (prednisolone > 7.5mg/day for > 2 weeks prior to delivery):
ďź Give parenteral hydrocortisone 100mg 6-hourly to cover the stress of labour until oral
medication is restarted.
⢠Prostaglandin E2 (Prostin) may safely be used for induction - not associated with
bronchospasm.
⢠All forms of pain relief may be used safely.
⢠Syntometrine may be used with caution for PPH prophylaxis(Ergometrine can cause
bronchospasm) .
⢠Avoid usage of labetalol in women with severe asthma.
28. Management: Post-Partum Care
⢠Encourage breastfeeding.
⢠Continue medications as usual - reassure about its safety in
breastfeeding.
⢠Ensure proper follow-up in Health Clinic or Chest Clinic.
⢠Contraception advice
29. Acute Exacerbation of Bronchial Asthma (AEBA)
⢠AEBA is dangerous and must be vigorously managed in the hospital.
⢠Treatment is no different from non-pregnant patients.
⢠Refer to medical team for further management. General management of AEBA:
ďź Relieve hypoxaemia - give high flow O2, maintain SpO2> 95%.
ďź Relieve bronchospasm-
o B2-agonists nebulisation (repeated doses or continuous nebulisation may be indicated for those with a poor
response)
o nebulised ipratropium bromide (0.5 mg 4 - 6 hourly) should be added for severe or poorly responding asthma.
ďź Give steroid therapy - reduces mortality, relapses, subsequent hospital admission and requirement for B2-
agonists; the earlier it is given, the better the outcome; give IV hydrocortisone 100 mg 6-hourly or oral
prednisolone 40-50 mg for at least 5 days.
ďź Rehydration and correction of electrolyte imbalance - B2-agonists and/or steroids can cause hypokalaemia.
⢠Do CXR with abdominal shield for:
ďź Suspected pneumonia or pneumothorax
ďź Poor treatment response
ďź Requiring ventilation
Refer for intensive care:
ďź If deteriorating PEFR, persisting hypoxia, hypercapnia,acidosis, exhaustion, feeble respiration, drowsiness,
confusion, coma, respiratory arrest.
ďź Consider IV B2-agonists or IV MgS04 or IV aminophylline in patient with life threatening / acute severe AEBA who
fails to respond to initial therapy.
31. Case Scenario
20 years old female, 17w 2d POA
⢠Presented with
⢠Worsening bilateral pedal edema and periorbital edema x1/52
⢠Persistent dry cough x 1/52
⢠Orthopnea (need to use 2 pillows) x4/7
⢠SOB, epigastric pain, vomiting and diarrhoea, epigastric pain, tea- coloured
urine and oliguria for x2/7
⢠Otherwise, no PND, palpitation or chest pain
32. ANC
1. SLE
Diagnosed 1 year ago, presented with
- Alopecia, Malar rash, Discoid rash, Oral ulcer, On and off fever, Joint
pain and swelling of bilateral hands
- ANA (+4) homogenous 1:80, leukopenia, anemia, lymphopenia, BUN
(N), Crea (N), Proteinuria(++)
- Under rheumato follow up
- Patient discontinued prednisolone for past 2 months by herself
33. Examination
⢠O/E, alert, slightly pale conjunctivae, anicteric sclera, bilateral
periorbital edema
⢠BP 140/80, PR 110, RR 24, T 38C
⢠Lungs: Equal chest expansion,equal breath sounds bilaterally,
no crackles/wheeze
⢠Cardiovascular: S1S2, No murmur, apex beat @ 5th ICL MCL
⢠Abdomen: soft, epigastric tenderness, not distended, no
mass/organomegaly, SFH = 20 cm, FHR : 152
⢠Bilateral pitting pedal edema
⢠No active dermatoses
34. Investigations
⢠Significant proteinuria on urinalysis and 24hr urine collection with
with fine and coarse casts
⢠Raised creatinine
⢠ABG: metabolic acidosis
⢠CXR: bilateral pleural effusion and cardiomegaly
⢠ECHO: moderate pericardial effusion, RA and RV wall collapse, fair LV
systolic function
⢠Hb: 8.2g/dL
36. Introduction
⢠The prevalence of SLE in women of childbearing years is around 1 in
500
⢠Pregnancy (and particularly the puerperium) increases the likelihood
of flare, from about 40% to 60%, which may occur at any stage of
pregnancy or the puerperium.
⢠Clinical features- joint involvement (90%), mucocutaneous (80%),
serositis, renal involvement, neurological and haematological
manifestation
37.
38. Pre pregnancy counselling
⢠Assessment for disease activity and the presence of any organ system involvement
⢠Presence of anti-Ro/La and antiphospholipid antibodies (associated with congenital heart block and neonatal
cutaneous lupus syndrome)
⢠Antiphospholipid antibodies are present in about 30% of women with SLE and are associated with arterial
and venous thrombosis, recurrent miscarriage, fetal growth restriction, fetal loss and preterm delivery due
to uteroplacental insufficiency
⢠Advise not to conceive during a period of active disease, particularly with lupus nephritis (2-4 folds hinger
incidence of pre-eclampsia, preterm delivery and fetal growth restriction)
⢠Active lupus nephritis may require to use such treatments as cyclophosphamide and mycophenolate mofetil,
which are associated with congenital malformations if used in the first trimester
⢠Review medication:
⢠NSAID may interfere with blastocyst implantation
⢠Substitite ACE inhibitor to appropriate anti-HPT
⢠Continue hydroxychloroquine and corticosteroid & azathioprine are safe in pregnancy
⢠Avoid teratogenic (mycophenolate) and discontinue cytotoxic (methotrexate, cyclophosphamide) 3 months prior to
conception
39.
40. Antenatal care
⢠Multidisciplinary team â combined clinic
⢠Establish baseline values:
⢠Renal status- BP, urinalysis, baseline 24-hour urine protein, renal profile, renal biopsy (if any) result.
⢠Haematology status- FBC with white cell differentiation.
⢠Maternal and fetal risk- anti-dsDNA, complement titres, anti-Ro/La.
⢠Pregnant women with active SLE/lupus nephritis or anti-Ro/ La/antiphospholipid antibodies should be
considered as a higher risk group
⢠For those individuals with stable disease, 4-weekly reviews of disease activity and regular assessment of fetal
growth, blood pressure and proteinuria are appropriate.
⢠For patients with anti-Ro/La positive the fetal heart rate should be monitored and recorded at each visit and
fetal echocardiography assessments made at 18â20 and ~28 weeks of gestation.
⢠Offer anomaly scan at 18-22 weeks if risk for fetal anomaly (exposure to cyto toxic drugs)
⢠Actively treat flares with corticosteroids according to its severity (liaise with physician)
⢠Patients with concurrent APS or previous venous thromboembolism should receive thromboprophylaxis with
low molecular weight heparin throughout pregnancy and for 6 weeks postpartum
41. Be aware of symptoms overlap between normal pregnancy and SLE flare and between
lupus nephritis and pre eclampsia.
42. Intrapartum
⢠Aim for vaginal delivery, CS is for obstetric indication.
⢠If suspected fetus with congenital heart block â deliver in centre with
paediatric cardiology facility.
⢠Patients on oral steroids (prednisolone > 7.5mg/ day for > 2 weeks
prior to delivery)
⢠Give parenteral hydrocortisone 100mg 6-hourly to cover the stress of labour
until oral medication is restarted.
43. Post Partum
⢠Check baby for neonatal lupus:
⢠Most common is cutaneous lupus - usually manifest in 1st 2 weeks of life.
⢠Most serious is CHB - appears in utero, is permanent, and may be fatal (15-30%
mortality).
⢠All neonates born to mothers with anti-Ro/La should be referred to paediatric team
and get ECG done.
⢠Reassure mothers on the safety of corticosteroids, azathioprine and
hydroxychloroquine during breastfeeding.
⢠If patient need cytotoxic drugs (methotrexate, cyclophosphamide) - no
breastfeeding and advice patient on strict contraception.
⢠Contraception advice. Avoid COCP in women with active or flare of SLE or
at high risk of thrombosis.
⢠Arrange for follow-up under physician clinic.
44. Contraception
⢠Contraceptive choice in patients with systemic lupus erythematosus (SLE) and
antiphospholipid syndrome (APS) is challenging but important.
⢠Long-acting forms of contraception such as the progesterone intrauterine device
(IUD) or subdermal implant are preferable for most patients.
⢠Estrogen-containing hormonal contraceptives may be used in stable, inactive
SLE patients but are contraindicated in patients with positive antiphospholipid
antibodies or with active or flare of SLE.
⢠The levonorgestrel IUD is a good alternative for many APS patients and often
decreases menstrual blood loss.
⢠It is prudent to avoid depot medroxyprogesterone acetate (DMPA) in
corticosteroid-treated or other patients at risk for osteoporosis because of the
inhibition of ovulation.
⢠Effective and safe contraception in patients with SLE and APS permits planning
for pregnancy during inactive disease and while on pregnancy-compatible
medications, preventing a poorly timed pregnancy that may jeopardize maternal
and/or fetal health.
46. Madam Heather
35 y/o G2P0+1 @20 W POG, NKMI other than a h/o childhood asthma
p/w SOB on exertion for the past 3 days. Booking history revealed a
baseline HR of 47/min, o/w all other parameters were normal. She had
a complete miscarriage 3 years back, no D&C done, o/w all other
history were insignificant
Upon examination, sheâs comfortable at rest, not tachhypnic, BP
110/70, HR 45, afebrile, SPO2 98% on RA, Daptone shows a FHR of 135
48. Subsequent management
Referred to cardiologist for an urgent ECHO
Subsequent ECHO findings: dilated right atrium and ventricle, left ventricular
hypertrophy (LVEF 30%)and mild regurgitations in all cardiac valves.
Multidisciplinary meeting was called. In the meeting, she was given 2 options:
Option 1: with her poor cardiac function, terminate said pregnancy
Option 2: Pacemaker insertion and carry out the pregnancy, with an Elective
Caesarean Section planned at 38w
outcome: She chose option 2, pregnancy was uneventful. Pacemaker
insertion done at 24w, subsequently was well. Elective Caesarean section at
38w, subsquently she was discharged day 2 post Caesar.
49. Classification of heart disease (CHD)
NON-CYANOTIC
⢠Abnormal shunting, eg ASD,VSD,PDA
⢠Out flow tract obstruction,eg coarcation of aorta,AS,PS
ACQUIRED DISEASE
⢠Rheumatic heart disease ,MS,MR,AS,AR
⢠Myocardial infarction
50. CYANOTIC
⢠Tetralogy of Fallot,pulmonary atresia
⢠Transposition of great arteries
INHERITED CONDITIONS
⢠MVP,Marfanâs syndrome
⢠Hypertrophic cardiomyopathy
CARDIOMYOPATHIES (CM)
⢠Peripartum CM
⢠Dilated CM
51. Pre-Pregnancy Care
⢠History of heart disease,arrhythmia,TIA
⢠History âsymptoms (NYHA class III&IV)
⢠Examination âcyanosis (Sao2<80%)
⢠Investigation LVEF <40% (myocardial dysfunction),left heart
obstruction(mitral valve area <2cm2,aortic valve area <1.5cm,aortic
valve gradient>30mmhg,presence of pulmonary hypertension
52.
53. Risk stratification based on the modified WHO and
NYHA classification
MATERNAL CV RISK WHO CLASS NYHA CLASS
Low risk I & II I & II
Moderate risk II-III&III --
High risk IV III & IV
54. Discuss with patient and her next of kin
⢠Effect of pregnancy on disease-risk of deterioration ,maternal risk of
morbidity/mortality
⢠Effect of disease of pregnancy-fetal risk (fetal loss,preterm
birth,LWB,CHD recurrence,teratogenic drugs,maternal risk and
pregnancy outcome
⢠Contraception advice:
Encourage planned pregnancy âappropriate timing of pregnancy
Avoid pregnancy in high risk patients
55. Optimize the cardiac function and minimize the risk first-to consider op
before pregnancy
Drugs-avoid teratogens (substitute with safer alternative)if possible
advise on pros and cons of anticoagulant
Other general measures:
Treat the U/L like HTN,DM,stop unhealthy lifestyle
Dental review-stress importance of dental hygiene
Folic acid supplements(ideally at least 3months pre-conception)
Advice booking at nearest clinic as soon as pregnancy is suspected
56. Management: Antenatal care
At booking visit
Do clinical assessment
History & physical examination
Drug history
Baseline investigations (if necessary)
Do risk stratification (WHO & NYHA)
57. Low risk
⢠Primary care: Local healthcare facility-MO & FMS
⢠Refer combined clinic : seen at least once within 1st trimester or at
least by 18weeks to formulate individualized âpregnancy care planâ
Moderate risk
Refer cardiac expert,combined clinic for âpregnancy care planâ
Close maternal-fetal surveillance
Anaesthetic review in advance
58. High risk
⢠Early Termination of pregnancy ,up to 22 weeks
⢠Anomaly scan at 18-22 weeks for patients with CHD
⢠Treat the underlying factors for maternal like
infections,anaemia,arrhythmias,HPT,DM dental caries
⢠Admission to ward for high risk/cyanotic patients who decine TOP
59. INTRA-PARTUM CARE
⢠Multidisciplinary team management
⢠Aim for vaginal delivery (less blood loss and infection)
âinduced(avoid long induction time)
-if high risk then should deliver in tertiary centre
C-section
For patients with;
-oral anticoagulants who have not been switched to heparin
-Marfan syndrome,aortic diameter > 45mm
-Acute/chronic aortic dissection
-NYHA III & IV
-LVEF <30%
-Severe obstructive cardiac lesions
-Severe pulmonary hypertension and Eisenmenger syndrome
60. Post âPartum care
⢠moderate/high risk patients
-Monitor in HDU/ICU for the first 24-72 hours
-monitor fluid overload
-3-5days of stay,if with pulmonary hypertension 7-14days of stay
-recommenced medication as indicated
-encourage early mobilization
-for anticoagulants if indicated( for PE care and to achieve INR care
before discharge)
-TCA in cardiac clinic and contraception advice
61. Contraception
⢠Ideally: Progestrone-only Pills or IM Depoprovera or Permanent
Sterilisation
⢠OCPs can cause VTE
⢠IUCD can cause endocarditis
⢠Barrier methods have high failure rates
62. Indications for TOP
⢠Eisenmengerâs syndrome
⢠Marfanâs Syndrome with Aortic involvement
⢠Severe pulmonary hypertension
⢠Coarctation of aorta with valvular involvement
66. Epilepsy in Pregnancy
⢠60% of women will experience no change in seizure frequency during
pregnancy,
⢠30% increased frequency
⢠10% decreased frequency.
⢠Although the increased seizure frequency in some women may be
due to pregnancy-related fall in plasma drug concentrations, other
factors such as sleep deprivation, poor compliance, inappropriate
reduction in AED therapy and vomiting may also contribute.
67. ⢠Pregnancy does not increase the risk of developing new epileptic
seizures for the first time.
⢠However, if seizures do develop de novo in pregnancy, certain special
causes must be considered and appropriately ruled out because they
are more common in pregnancy.
⢠A brain MRI or CT with lead shielding will ofte be required
68. Special causes of epilepsy developing in
pregnancy
⢠Enlarging meningioma
⢠Enlarging arteriovenous malformation
⢠Ischaemic stroke
⢠Cerebral venous or venous sinus thrombosis
⢠Vasculitides
⢠Subarachnoid haemorrhage
⢠Eclampsia
70. Pre-conception management and counselling
⢠Ideally, women should be advised against getting pregnant until they become seizure free
and are off AEDs.
⢠However, for various personal, cultural or religious reasons, this is seldom possible or
practical.
⢠The goal is to:
⢠minimise risk of teratogenicity and seizure control
⢠by switiching (if able to) to monotherapy or using Antiepilpetics that are less teratogenic
⢠The risk is low if the patient has been seizure-free for more than 2 years and tapering is done
gradually.
⢠Switching to a less teratogenic AED should be done before conception; switching during
pregnancy is likely to be pointless because most teratogenic effects take place in the first
trimester.
⢠For the above reason, contraception should be practiced till AED adjustment is achieved.
⢠In cases where a patient with epilepsy is on AEDs and is seen for the first time in the first
trimester, the AEDs should not be stopped or regime modified if the seizure control is good
(rare attacks or complete seizure freedom).
71.
72. Labour
⢠The risk of seizures is greatest during the delivery period; 1-2% of epileptic
women suffer a GTCS during labour. This must be made known to the patient
and her obstetrician so that necessary precautions can be taken.
⢠The patientâs regular AEDs must be continued through labour, via a nasogastric
tube or intravenously, if necessary.
⢠As pain, emotional stress and hyperventilation may increase the risk of seizures,
epidural anaesthesia should be considered early during labour.
⢠If frequent GTCS or complex partial seizures do occur during labour, a caesarean
section is indicated.
⢠An elective caesarean section is also recommended if frequent GTCS or complex
partial seizures occur during the last weeks of pregnancy; the treatment of the
seizure itself should proceed in the usual manner.
73. Contraception
⢠There is an increased risk of oral contraceptive pill (OCP) failure with AEDs that
induce hepatic microsomal enzymes (barbiturates, phenytoin, carbamazepine,
and oxcarbazepine) These drugs enhance hepatic metabolism of contraceptive
steroids and reduce their biologically active compound.
⢠Patients on the OCP need to be advised about additional non-hormonal
contraceptive measures. If a woman wishes to rely on the OCP alone, she
should be prescribed a preparation containing a higher amount ( at least 50 Âľg
of oestradiol), as opposed to the commonly available OCPs .
⢠Intramuscular Depo-Provera at a dose of 150 mg should be given at shorter
intervals (every 10 weeks instead of 12 weeks) if she is on enzyme-inducing
AED.
⢠There is no evidence that hormonal contraception adversely affects seizure
control, except for those patients treated with lamotrigine whose metabolism is
significantly increased by OCP.
74.
75. Important Steps in the Management of Pregnant
Women with Epilepsy
⢠Preconception counselling of the patient about risks of teratogenicity
and possible adverse effects of uncontrolled seizures to maternal health
and pregnancy
⢠Preconception review of AEDs; aim for minimal effective monotherapy if
active epilepsy; consider drug withdrawal if seizure free
⢠Commence preconception folic acid supplements
⢠Screen for malformations
⢠Monitor condition and AED concentrations throughout pregnancy
⢠Reassure patient that >90% pregnancies proceed with no problem in
women with epilepsy