Thyroid Disease in PregnancyThyroid Function in normal pregnancy:
• increased Thyroid Binding Globulin
production. This leads to an increase in
total T 4 and T 3 , but not the free
circulating thyroid hormones.
• iodine deficiency in pregnancy:– increased glomerular filtration
– fetal thyroid activity.
This results in increased uptake by the
thyroid gland which enlarge and goitre
• As human chorionic gonadotrophin(hCG) and TSH share a common alpha
subunit and have similar beta subunits,
TSH receptors are prone to stimulation by
Fetal thyroid function:• From 10 weeks' gestation, the fetal
thyroid gland produces both T 4 and T 3
Fetal levels reach those of the adult at 16
• Congenital hyperthyroidism can occur
through TSH receptor stimulating
antibodies which cross the placenta.
Iodine Deficiency:• In iodine deficiency, the maternal thyroid
gland has a greater affinity for iodide than
the placenta and the fetuses are thus
prone to cretinism, the leading
preventable cause of mental retardation
• The fetal cochlea, cerebral neocortex and basalganglia are particularly sensitive to iodine
• Iodine administrationprior to conception
and up to the 2 nd
trimester will improve
by protecting the fetal
brain. Iodination of
water, salt or flour can
easily achieve this.
Hyperthyroidism• occurs in approximately 1 in 500
pregnancies and is usually due to Graves'
• Disease severity is correlated to IgG
thyrotropin receptor stimulating antibody
• Typical signs of hyperthyroidism are
difficult to elicit in pregnancy, but poor
weight gain in the presence of a good
appetite or a tachycardia can aid Dx.
• Maternal and fetal complications includethyroid storm, heart failure and maternal
hypertension. Also increased rates of
premature labour, intrauterine growth
restriction and stillbirth.
Treatment:• radioactive iodine must not be given.
• Surgery may be considered if medical
treatment fails or there is a clinical suspicion
of cancer or compressive symptoms due to a
• Medical treatment involvespropylthiouracil PTU and carbimazole.
Both drugs cross the placenta in the same
proportion & are equally beneficial and
the dose of either can be titrated against
maternal well - being and biochemical
• Neither PTU nor carbimazole is thought
to be teratogenic.
• It is recommended that thyroid function
tests be performed every 4 - 6 weeks.
Fetal hyperthyroidism• When maternal thyrotropin receptor
stimulating antibodies cross the placenta, they
can cause fetal or neonatal thyrotoxicosis. The
fetal thyroid is capable of responding to these
antibodies after 20 weeks' gestation.
• Assessment include maternal perceptionof fetal movements and measurement of
the fetal heart rate, which is > 160 bpm.
An ultrasound scan used to exclude a
fetal goitre or fetal growth restriction.
• In suspected cases cordocentesis for freeT 4 & TSH estimation can be performed.
• Complications includePremature delivery,
hydrops fetalis and
• fetal goitre can cause
polyhydramnios and an
• The condition is also
• The fetus can be effectively treated bymaternal administration of anti thyroid agents,
which cross the placenta. The fetal heart rate
can be used to titrate the dose of anti thyroid
Hypothyroidism:• Incidence: 1 % of pregnant women and is
usually due to autoimmune Hashimoto's
thyroiditis or idiopathic myxoedema.
• There is a reduced IQ in babies of women with
hypothyroidism that are not adequately treated,
or that goes unrecognized. The insult is likely
to occur in the first trimester, and therefore
pre - conceptual optimization of T 4 therapy is
• The classical symptoms of hypothyroidism arecommon to pregnancy and cannot be relied
upon to discriminate onset or worsening of the
disease. The management is therefore based
principally on biochemical measures.
• Thyroxine is titrated against biochemical
results and is safe in pregnancy and lactation.
As long as the patient is clinically euthyroid,
thyroid function test should be performed
every 2 - 3 months.
Postpartum thyroiditis:• occur up to a year following delivery and
can manifest as high or low T 4 levels.
• Associated with thyroid antiperoxidase
antibodies. Histology suggests a chronic
thyroiditis with lymphocytic infiltration.
• The disease may present initially between
1 and 3 months postpartum with
thyrotoxicosis and later with
• Hyperthyroidism is due to destruction ofthyroid follicles & release of preformed
hormones. The destruction of thyroid
follicles ultimately leads to hypothyroid
phase. A course of T 4 may be necessary.
• The period of hypothyroid state is variable,
and permanent hypothyroidism can result.
• The condition may recur in future
pregnancies and follow up is needed to
ensure that permanent hypothyroidism does
• Incidence : 1 in 200 pregnancies
Pre -pregnancy counselling
• Alter medication according to seizure frequency
• Reduce to monotherapy where possible & ensure
• Pre -conceptional folic acid 5 mg
• Explain risk of congenital malformation:anticonvulsant medications are associated
with a two - to three -fold increased risk of fetal
• Explain risk from recurrent seizures
• Many factors contribute to altered drug metabolismin pregnancy and result in a fall in anticonvulsant
• The reasons for increased fit frequency in
pregnancy therefore include:
the effect of pregnancy on the metabolism of
sleep deprivation or stress
poor compliance with medication .
• Delivery mode and timing is largely unaltered byepilepsy
• Anticonvulsant medication should be continued
• Newborn should receive Vit K 1 mg IM to avoid
haemorrhagic disease of newborn
• Breastfeeding can be encouraged, feeding is best
avoided for a few hours after taking medication.
• Information on safe handling of the neonate should
be given to all epileptic mothers.
Causes of seizures in pregnancy• Epilepsy
• Encephalitis or meningitis
• Space -occupying lesions (e.g. tumour, tuberculoma)
• Cerebral vascular accident
• Cerebral malaria or toxoplasmosis
• Thrombotic thrombocytopenic purpura
• Drug and alcohol withdrawal
• Toxic overdose
• Metabolic abnormalities (e.g. hypoglycaemia