Thyroid disorders during

pregnancy
Reproductive block 5th year
2020-2021
‫من اقوال االمام علي (ع) في العلم‬
‫• " كل وعا ٍء يضيق بما ُجع َل فيه اال وعاء العلم ‪ ،‬فانه يتّسع " ‪.‬‬

‫علم وطالب دنيا " ‪.‬‬

‫طالب ٍ‬
‫ُ‬ ‫• و " منهومان ال يشبعان ‪:‬‬

‫• و " ما مات من أحيا علما ً وال افتقر من َملَ َك فهما ً " ‪.‬‬

‫• و " وتعلموا العلم صغاراً تسودوا به كباراً " ‪.‬‬

‫• و " الجاهل صغير وان كان شيخا ‪ ،‬والعالم كبير وان كان حدثا ً " ‪.‬‬

‫• و " األنس بالعلم من نبل اله ّمة " ‪.‬‬

 Overview
• Thyroid diseases are common in women of child bearing
age
• Many of symptoms of thyroid diseases resemble those of
normal pregnancy.????????
What are the physiological changes in pregnancy that affect
thyroid function?
Diagnosis of thyroid disorders :
1. H/E
2. Ix.
Mention the useful tests to assess thyroid function during
pregnancy?
 Thyroid physiology during pregnancy
• Serum levels of TBG, total and bound thyroid hormons are incr.
• TSH in early pregnancy decr. Due to incr. Placental hCG. ( so free thyroxin
incr. at 1st 12 weeks which inhibits TRH then TSH).
• TSH has no direct fetal effect because it does not cross the placenta.
• At mid pregnancy TRH levels are found in fetus but remain static.
• Maternal thyroxin is transferred to fetus ( important in fetal brain development).
• Fetal thyroid begins concentrating iodine and synthesizing thyroxin after 12
weeks.
• Maternal sources account for more than 30% of thyroxin in fetal serum at term.
 Autoimmunity and thyroid diseases
• Most of thyroid disorders are linked to autoantibodies.
• Effect of these antibodies either: stimulate thyroid function, block function, or
cause thyroid inflammation.
1. Thyroid stimulating autoantibodies (TSIs): bind to TSH receptors causing
activation then hyperfunction and growth. ( in Grave’s disease)
2. Thyroid peroxidase: is a normal enzyme in the production of thyroid hormons.
Autoantibodies are directed toward it leading to dysfunction. (may be linked
to early pregnancy loss). Also associated with abruption, postpartum thyroid
dysfunction and lifelong thyroid failure.
 Different presentations
fT4 TSH Condition

L H Overt hypothyroidism

Normal range H Subclinical hypothyroidism

H undetectable) Overt hyperthyroidism

Normal range L Subclinical hyperthyroidism

 Investigations of thyroid disorders
• Typically a TSH and free T4 are required to make the diagnosis for the vast majority of
thyroid disorders.

• Free T3: When there is a strong clinical suspicion for thyroid disease with an abnormal
TSH and free T4 evaluation is unremarkable.

• Thyroid-stimulating immunoglobulins(TSI)are the pathologic antibodies found in

Graves’ disease-related hyperthyroidism that They can be used to confirm the
diagnosis.

• Antithyroid peroxidase antibodies (TPO)are antibodies commonly associated with

Hashimoto disease and hypothyroidism. TPO antibodies in euthyroid women have been
associated with future thyroiditis risks as well as pregnancy loss. TPO testing may be
indicated in women with recurrent pregnancy loss
 Hypothyroidism
• Incidence 1% of pregnants ( 2-10/1000)
• The most common cause of hypothyroidism during pregnancy is Hashimoto’s
thyroiditis ccc by glandular destruction by autoantibodies (antithyroid peroxidase
antibodies)
• Another cause is postablative Grave’s disease.
• Severe hypothyroidism in pregnancy is uncommon(usually associated with
subfertility and higher spontaneous abortion rates)
• Dx is difficult during pregnancy???
• When Dx made during pregnancy ( low thyroxin and high TSH) , Tx should be
continued throughout pregnancy (aim is less than 4 mmol/l)
• SUBCLINICAL HYPOTHYROIDISM is ccc by high TSH and normal thyroxin
 Management
Prepregnancy:
• Reassurance about the safety of thyroxin use during pregnancy.
• Pt with hypothyroidism should be counseled to delay pregnancy until maintenance levels of T4 are achieved.
• It is useful to perform baseline TSH and T4 in women who plan for pregnancy in near future or as early as
possible in pregnancy.
Antenatally:
• TFT should be performed as early as poosible then at each trimester or more often if dose adjustments are
required.
• Using of pregnancy-specific ranges for interpreting results.
• Those who enter pregnancy euthyroid, may expect a good outcome.
• Treatment with thyroxine initially 100 micrograms daily (1-2 microgram/kg/day) and checking thyroid
function each Tx if stable.
• Avoid taking iron supplements at the same time and Check compliance in pt with vomiting.
Describe the effects of suboptimal thyroid replacement on the fetus???
May be associated with developmental delay and pregnancy loss therefore; Maternal T4 levels are more important
 Treatment
• Greater thyroxine requirement is at 5 wk of pregnancy
• Incr thyroxine demands in about 1/3 of supplemented pregnant
women (due to augmented estrogen production).
• Significant hypothyroidism may develop in women with low thyroid
reserve as in: those with thyroidectomy, prior radioactive iodine and
those with ART (require 25% incr in thyroxine dose at confirmation of
pregnancy).
• Dosing typically increases in the first trimester
Mx of labour and delivery:
1. With adequate control, no specific measures are needed
2. When a large goitre is present, anesthetic complications (difficult
intubation, and respiratory compromise) may occur and require
surgical or anesthetic advice.
 In the postpartum period levothyroxine dosing should be returned
to prepregnancy levels, screen for thyroiditis and depression.
 Pregnancy outcomes
• Spontaneous miscarriage and fetal demise
• Placental abruption
• Gestational hypertension and preeclampsia
• Preterm delivery
• Offspring developmental delay
• Low birth weight
• Fetal hypothyroidism in about 1/180.000 newborn
 Iodine deficiency
• Dietary iodine requirements are higher in pregnancy due to: augmented thyroid
hormones production, incr renal losses, and incr fetal demands.
• Adequate iodine is mandatory for fetal neurological development beginning soon
after conception.
• Abnormalities depend on degree of deficiency: mild deficiency (doubtful)
• Severe deficiency frequently associated with damage ( as in endemic cretinism).
• Moderate deficiency has intermediate and variable effects.
• Endocrine Society recommends intake of 150 micrg of iodine in reproductive-age
women incre up to 250 micrg during pregnancy and lactation.
• Avoid exceeding 500 micrgr/ day ( may lead to subclinical hypothyroidism and
autoimune thyroditis).
 Hyperthyroidism
thyrotoxicosis in pregnancy
• Grave’s disease (autoimmune thyroiditis) affects about 2/1000
pregnancies.
• Usually Dx before pregnancy
• In early pregnancy, the symptoms initially worsen due to incr. hCG (or
due to decreased absorption of medications as a result of vomiting)
then decr. in the 2nd half of pregnancy (due to decr. Antibody titres).
 Diagnosis
1) S&S:
Palpitations, tachycardia, thyromegally, heat intolerance and palmar erythema,
all of which can also be seen in normal pregnancy. Eye signs (exophthalmous)
and pre‐tibial myxoedema are specific to autoimmune thyroid disease and
weight loss does not occur in normal pregnancy.
2) Lab tests ( confirmatory)
High levels of T4 and suppressed TSH
Rarely hyperthyroidism can be caused by abnormally serum T3 level - called T3
toxicosis.
Presence of TSIs which are used for Dx , Mx, & prognosis. These receptor
autoantibodies are reserved for cases in which fetal thyrotoxicosis is suspected.
 Management
• Treatment best begun before pregnancy to allow for the use of radioactive iodine studies for Dx, higher
initial doses of drugs without concern about fetal effects, and surgery for pt does not respond to Tx.
• Antenatally, the aim of Tx is to maintain maternal fT3 and fT4 levels in the high / normal range
while TSH remains suppressed.
• Serum free T4 levels are measured every 4-6 weeks (or more frequently if needed).
• Perform fetal uls for fetal growth, tachycardia or goitre.
• Women with autoimmune thyroid disease should have TSH receptor antibodies checked as they can
cross the placenta and stimulate the fetal thyroid.
• In adequately treated pt, no incre risk during labour or delivery.
• Postnatally Symptoms may worsen especially if Tx is reduced.
• TFT should be performed on umbilical cord blood and in neonates in women who are breastfeeding
and observing for the signs of hypothyroidism
• Carbimazole and propylthiouracil can be given to lactating women. No neonatal concerns if given in
small doses, but monitoring required in high doses.
 Treatment options

• Medical by
1. Either carbimazole or PTU (preferred) using the lowest possible
cause. Why ??????
Regular check of maternal WBCs is mandatory. WHY???
List the side effects of the above drugs….
2. Beta-blockers can be used initially
• Radioactive iodine is CI. WHY??????
• Surgical. Highlight the indications????
 Indications of subtotal thyroidectomy

• Can be performed after medical control of thyrotoxicosis.

• Rarely done during pregnancy ( best performed in 2nd Tx).
• Indicated in women with no response to medical treatment
or in whom treatment is proved toxic.
• Pressure symptoms.
 Side effects of antithyroid drugs
• Methimazole associated embryopathy ( esophageal or choanal atresia and
aplasia cutis)
• Transient leucopenia in 10%
• Agranulocytosis in 0.3-0.4%
• Hepatotoxicity in 0.1-0.2% (mostly with PTU)
• antineutrophil cytoplasmic antibodies with PTU ( 20%)
• Vasculitis.
 What are the adverse effects of uncontrolled thyrotoxicosis?

• Pregnancy outcomes: depends on Fetal and neonatal effects:

metabolic control) Perinatal mortality 6-12%
Miscarriage Preterm labour
Placental abruption IUGR
Preeclampsia Clinical hyperthyroidism in neonate in 1%
Thyroid storm and / or Heart failure Goitrous thyrotoxicosis
Non- immune hydrops.
Woman with clinical hyperthyroidism has
Goitrous hypothyroidism ( due to fetal
12- folds risk of delivering infants with
exposure to maternally ingested
hearing loss.
thionamides)
 Thyroid storm
• Life-threatening event ( rare in pregnancy)
• Can be fatal in 20-50% of untreated cases.
• Causes: underTX, infection, labour
• Dx: Hx, EX, TFT
• Tx:
• Mx in intensive care unit
• supportive care,
• PTU,
• Iodide is given after 1-2 hrs from thionamide Tx ( to inhibit release of T4 & T3).
• Steroids ( IV dexamethasone 2mg every 6 hrs for 4 doses to block conversion of T4 to T3)
• Beta blockers
• Coexsisting conditions (PE, anemia, and infection should be Tx before delivery)
 Other types of hyperthyroidism
• HEG and gestational transient thyrotoxicosis: 2 -15%, results from TSH-
receptor stimulation from normal for pregnancy HCG. Do not require tx. TSH
and thyroxin become normal at mid pregnancy.
• Thyrotoxicosis and GTD: in 25-65%. High level of HCG leads to
overstimulation of TSH receptors. The level normalizes in parallel with HCG
decr.
• Subclinical hypertoxicosis: ccc by abnormally low TSH, with normal thyroxin
level. Long term effects: osteoporosis, cardiovascular morbidity, overt
thyrotoxicosis, thyroid failure,
 Postpartum thyroiditis (Transient
autoimmune thyroiditis)
• Found in about 5-10% in the 1st year after child birth
• More in pt with IDDM, Fhx of disease, or TPO
• Most cases resolve spontaneously
• Risk of recurrence???????
• Includes hyperthyroidism, hypothyroidism or both
• 50% of women who are thyroid-antibody positive during the 1st Tx will develop postpartum thyroiditis.
The Dx is infrequent because it develops months after delivery and has nonspecific symptoms.
Classically has 2 phases:
1. Destruction-induced thyrotoxicosis: the earliest phase with abrupt onset. Symptoms are due tocessive
release of thyroid h from glandular disruption. Small painless goiter. Fatigue and palpitations are more
common. This phase lasts few months. Thionamides are ineffective and if symptoms are severe, B-blockers
may be given.
2. Hypothyroidism from thyroiditis: starts bet 4-8 months postpartum.
Thyromegaly and other symptoms are more prominent than in thyrotoxic phase.
Thyroxine 25-75 micrgr/d is given for 6-12 months.
• Women with either type of postpartum thyroiditis have 20-30% risk of
developing permanent hypothyroidism (annual progression rate is 3.6%)
• Women at greater risk for developing hypothyroidism are:
Those with higher titres of thyroid Ab
Those with higher TSH level at initial hypothyroid phase.
• Other may develop subclinical disease.