Thyroid disorders are common in pregnancy and can impact both mother and baby if not properly managed. Hyperthyroidism, hypothyroidism, and postpartum thyroid disease are the main thyroid conditions seen. Treatment involves medication like antithyroid drugs, levothyroxine, and beta blockers with careful monitoring of thyroid levels throughout pregnancy. Screening high-risk women and optimizing thyroid function is important for achieving good pregnancy outcomes.
Introduction
• Most commonendocrine
disorder in pregnancy.
• Affects 1-2% pregnant
women.
• Pregnancy may modify
course of thyroid disease.
• Pregnancy outcome can
depend on optimal
management of thyroid
disorders.
4.
Iodine requirement inpregnancy
Iodine requirement increases in pregnancy due to –
• Increase thyroid hormone production
• Increase renal excreation
• Increase demand of fetus
5.
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ATA 2017-
•150 mcg/dayduring planing for pregnancy
•220 mcg/day during pregnancy
•290 mcg/day during lactation
WHO –
•250 mcg/day during pregnancy & lactation
7.
Physiological changes during
pregnancy
•Increase TBG –
• 2nd ary to increase
estrogenic stimulation &
reduced hepatic clearance of
TBG.
• TT3,TT4 increases.
• FT3, FT4 increase in 1st
trimester in response to elevated
HCG
8.
• hCG –
•Intrinsic thyrotropic activity
• Begins shortly after gestation, peaks at 10 wks,
declines at 20 wks
• Activates thyroid receptor
• Transient decrease of tsh during 8-11 wks due
to peak in hCG
Trimester specific TSHlevel
If trimester specific referance range is not
available in laboratory following referance
range is recommonded.
•1st trimester : 0.1 – 2.5mIU/L
•2nd trimester : 0.2 – 3.0 mIU/L
•3rd trimester : 0.3 – 3.5 mIU/L
12.
Who should testfor TFT during
pregnancy?
Targeted case finding vs Universal screening?
• ATA, AACE, ACE recommend screening high risk case
only.
• However different studies have shown upto 30%
cases missed in high risk screening .
ALL PREGNANT WOMEN SHOULD BE VERBALLY SCREENED AT
THE INITIAL PRENATAL VISIT FOR ANY HISTORY OF THYROID
DYSFUNCTION, AND PRIOR OR CURRENT USE OF EITHER
13.
All patients seekingpregnancy, or newly pregnant,
should undergo clinical evaluation. If any of the
following risk factors are identified, testing for
serum TSH is recommended.
• A history of hypothyroidism/hyperthyroidism or
current symptoms/signs of thyroid dysfunction
• Known thyroid antibody positivity or presence of a
goiter
• History of head or neck radiation or prior thyroid
surgery
• Age >30 years
14.
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• History ofpregnancy loss, preterm delivery, or
infertility
• Multiple prior pregnancies (2 or more)
• Family history of autoimmune thyroid disease or
thyroid dysfunction
• Morbid obesity (BMI 40 kg/m2 or more)
• Use of amiodarone or lithium, or recent
administration of iodinated radiologic contrast
• Residing in an area of known moderate to severe
iodine insufficiency
15.
Hyperthyroidism in pregnancy
•0.2% of all pregnancies
• Causes are-
• Graves disease
• Toxic MNG, toxic adenoma
• Sub acute thyroiditis
• Gestational trophoblastic tumor
• Geststional transient thyrotoxicosis
• Graves disease is most common ( 85%)
16.
Effects of hyperthyroidismin pregnancy
Maternal Foetal
Miscarriage hyperthyroidism
Abruptio placenta Prematurity
Preterm delivary IUGR
Congestive heart failure Still birth
Thyroid strom & Pre eclampsia
Thus there is an increase in maternal & perinatal
mortality
Graves disease inpregnancy
Sign & symptoms:
• Tachycardia, heat intolerance, anxiety, insomnia,
wt loss, goiter, frequent stool, fine tremor etc.
Graves specific sign:
• Diffuse goiter, expothalmous, pretibial myxedema.
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• Disease activityflactuates during pregnancy .
• Exacerbation during 1st trimester with gradual
improvement during later half.
• High risk of relapse during post partum.
20.
Gestational transient thyrotoxicosis
•Occurs in 1st trimester
• Due to HCG mediated stimulation of thyroid gland
• Thyroid gland usually not enlarged, no eye sign, no
prior history of thyroid disease, mild disorder &
associated emesis suggests transient thyrotoxicosis.
• Resolution of symptoms parallel to decline in hcg
level
• Usually resolves spontaneously by 20 wks
• If persists beyond 20 wks, repeat evaluation for
21.
Trophoblastic hyperthyroidism
• Associatedwith hydatidiform mole &
choriocarcinoma
• Nausea & vomiting predominant
• Unusual high hCG with snow strom
appearance on USG of L/A are found
22.
Diagnosis of hyperthyroidism
•TSH – decreased
• FT4,FT3 – increased
• TRAb – in GD ( when diagnostic uncertainity)
• Thyroid scan – contraindicated
• TT3, TT4 reference range should be adjusted at
1.5 times the non pregnant range
23.
Treatment options ofhyperthyroidism
•Anti thyroid drugs
(ATD).
•Beta blockers.
•Thyroidectomy ( rarely,
if needed done in 2nd
trimester).
24.
ATD
• ATD therapyshould be uesd for hyperthyroism in
pregnancy.
• In 1st trimester –propylthiouracil (PTU) – 100-
600mg/day
• 2nd & 3rd trimester – carbimazole(CM) - 10-
40mg/day
• Lowest possible dose should be used.
• Pt education about possible side effect of drugs
specially teratogenecity
• PTU – hepatoxicity
Beta blockers
• Betaadrenergic blocking agents, such as propranolol
10-40 mg every 6-8 hours may be used for
controlling hyper-metabolic symptoms until patients
have become euthyroid on ATD therapy. The dose
should be reduced as clinically indicated. In the vast
majority of cases the drug can be discontinued in 2
to 6 weeks.
• Long-term treatment with beta-blockers has been
associated with IUGR, fetal bradycardia and neonatal
hypoglycemia
27.
Monitoring
• Clinical S/Sof improvement.
• TSH, FT4/TT4 every 4 wkly.
• ATD dose has to be reduced when TSH is in
reference range to avoid fetal overtreatment.
28.
Hypothyroidism
• Untreated hypothyroidismis associated with sub
fertility, so hypothyroidism is uncommon in
pregnency.
• However the causes may be –
• Iodine deficiency
• Hashimoto thyroiditis
• Prior radio iodine therapy
• Prior thyroid surgery
29.
S/S of hypothyroidism
•Inappropriate wt gain
• Cold intolerance
• Dry skin
• Asthenia
• Hoarseness of voice
• HTN
• Constipation
Subclinical hypothyroism
• Suspectwhen TSH > 2.5mU/L & FT4 normal
• Increase risk of abruptio placenta, preterm baby
• Indication of treatment
• TPO (+)ve with TSH > pregnancy specific referance
range
• TPO (+)ve with TSH >2.5mU/L & below the upper limit
of pregnancy specific referance range
• TPO (-)ve with TSH > 10mU/L
• TPO (-)ve with TSH > pregnancy specific referance
range & below 10.0mU/L
34.
Treatment of hypothyroidism
•By oral Levothyroxin
• Levothyroxin should be administered as
2mcg/kg/day
• Usual starting dose 100mcg/day & then titrate.
• If already on Levothyroxin before pregnancy, on
confirmation of pregnancy increase dose by 30% (
20-50mcg)
• Never give FeSO4 simultaneously with thyroxin.
35.
Monitoring
• By TSHevery 4 wk until mid gestation, & at least
once near 30 wks of gestation ( ATA 2017)
• Target TSH < 2.5mU/L
• Target FT4 – upper end of normal
36.
Euthyroid & TPOAb(+) ve
• 2 times risk of miscarriage
• No risk of neonatal hypothyroidism
• Risk of developing overt
hypothyroidism as pregnancy
progress, so check TFT between 28-
32 wks of gestation
• Increase risk of post partum
thyroiditis ( check TFT at 3 month
post partum)
37.
Post-partum thyroid dysfunction
•Post-partum thyroiditis is the occurance of thyroid
dysfunction , excluding graves disease, in the 1st
postpartum year in woman who were euthyroid prior to
pregnancy. ( Ata 2017)
• Aetiology:
• Chronic autoimmune thyroiditis.
• Presentation: triphasic pattern
• Transient thyrotoxicosis ( 2-6 months)
• Transient hypothyroidism(3-12 months)
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• DD ofPPT:
• Graves disease that relapse in post patum
period
• Lymphocytic hypophysitis( rare)
• INVESTIGATION:
• TPO (+)ve in 80% case
• Thyroid scan to diferentiate from GD ( low
uptake in thyrotoxic phase of PPT, high uptake
in GD)
39.
Management
• Beta blockersif thyrotoxic & symptomatic until TFT
normalize. ATD not necessary.
• Levothyroxine if TSH > 10mU/L
• TSH 2.5-10mU/L with symptoms
• Prognosis:
• 25% recurrence in future pregnancies
• 30% permanent hypothyroidism within 10 yrs
41.
Thyroid cancer inpregnancy
• 2nd most common malignancy during pregnancy next to
breast cancer
• Thyroid nodules and thyroid cancer discovered during
pregnancy present unique challenges to both the clinician
and the mother.
• A careful balance is required between making a definitive
diagnosis and instituting treatment while avoiding
interventions that may adversely impact the mother, the
health of the fetus, or the maintenance of the pregnancy.
42.
Diagnostic approach forthyroid cancer
• History and physical examination
• The patient with a thyroid nodule should be asked
about a family history of benign or malignant
thyroid disease, familial medullary thyroid
carcinoma, multiple endocrine neoplasia type 2
(MEN 2), familial papillary thyroid carcinoma, and a
familial history of a tumor syndrome predisposing
to thyroid cancer syndrome.
• USG
• Most accurate tool for detecting nodule ,
determining sonographic features & pattern ,
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• Thyroid functiontests
• All women with a thyroid nodule should have a
TSH performed. Thyroid function tests are usually
normal in women with thyroid cancer
• Calcitonin and thyroglobulin
As within the general population, the routine
measurement of calcitonin remains controversial.
Calcitonin measurement may be performed in
pregnant women with a family history of medullary
thyroid carcinoma or multiple endocrine neoplasia 2
or a known RET gene mutation
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Fine needle aspiration
•Fine needle aspiration is a safe diagnostic tool
in pregnancy and may be performed in any
trimester
Radionueclide screening
• Containdicated
46.
Acknowledgment
• American thyroidassociation guidelines for the diagnosis
and management of thyroid disease during pregnancy and
the postpartum 2017, 2011
• Thyroid disease in pregnancy, practice bulletin
,number 223, june 2020,ACOG
• Davidson principles & practice of medicine 23rd edition
• Oxford handbook of endocrinology3rd edition