THYROID

DISEASE IN
PREGNANCY

THYROID DISEASE IN
PREGNANCY
Second most common endocrine disorder
Increased risk of miscarriage, placental abruption, hypertensive disorders,

and growth restriction.

 First trimester:
TSH decreases in early pregnancy because of weak stimulation of TSH receptors

caused by hCG during first 12 weeeks.

T4 will then supresses TSH at hypothalamic axis.
TSH return to baselines, and then increases in third trimester
Placental growth and production of placental deiodinase

Maternal T4 transferred to the

fetus is important for normal
fetal brain development.
(before the fetal thyroid gland
begins concentrating iodine
and synthesizing thyroid
hormone at approximately 12
weeks of gestation).

Levels of TSH
First Trimester: 0.12.5 mIU/L
Second Trimester: 0.2-3.0 mIU/L
Third Trimester: 0.3-3.0 mIU/L

SCREENING
personal hx of thyroid disease or sx of

thyroid disease,

autoimmune disease,
previous delivery of infant with thyroid

disease,

type 1 DM,
high dose neck radiation,
recurrent fetal loss

Universal screening not

recommended.

Not warranted for asymptomatic

pregnant women who have a

mildly enlarged thyroid (because
up to a 30% enlargement of the
thyroid gland is typical during
pregnancy)

HYPERTHRYODIS
M

HYPERTHYROIDISM
Occurs in 2% of pregnancy; Graves disease accounts of 95% of the cases.
Other causes: gestational trophoblastic disease, nodular goiter or solitary

toxic adenoma, viral thyroiditis, and tumors of the pituitary gland or ovary

Sx: nervousness, tremors, tachycardia, frequent stools, excessive

sweating, heat intolerance, weight loss, goiter, insomnia, palpitations, and

hypertension.

Symptoms similar to normal symptoms of pregnancy or some non-thyroid-

associated diseases, hence the results of serum thyroid function tests

differentiate thyroid disease from these other possibilities.

Maternal thyrotoxicosis is associated with a greater risk of severe

preeclampsia and maternal heart failure.

FETAL AND NEONATAL

EFFECTS HYPERTHYROIDISM
High risks of : Prem deliveries, low birth weight, and fetal loss.
Risk of development of immune-mediated hypothyroidism and

hyperthyroidism in the neonate. (antibody crosses placenta may stimulate

or inhibit fetal thyroid)

Neonates of women with Graves disease treated surgically or with

radioactive iodine are at high risk of neonatal Graves disease because they
lack suppresive thioamide. (Less incidence in patient on thioamide
treatment)

Routine evaluation of fetal thyroid function, including fetal thyroid

ultrasonographic assessment, umbilical cord blood sampling, or both, is not

recommended

SUBCLINICAL
HYPERTHYRODISM
1.7% of pregnant woman
Abnormally low TSH with normal T4
Not associated with adverse outcomes
Treatment is not recommended (antithyroid medications crosses placenta)

HYPOTHYROIDIS
M

HYPOTHYROIDISM
Overt hypothyroidism: 0.2-1% of pregnancy
Increased TSH with decreased T4
Sx: fatigue, constipation, cold intolerance, muscle cramps, and weight gain.
Clinically: edema, dry skin, hair loss, and a prolonged relaxation phase of

deep tendon reflexes, +/- Goiter

Hashimoto thyroiditis is the most common cause of hypothyroidism in

pregnancy and is characterized by glandular destruction by autoantibodies,

particularly antithyroid peroxidase antibodies.

Adverse perinatal outcomes: spontaneous abortion, preeclampsia, preterm

birth, abruptio placentae, and fetal death

FETAL AND NEONATAL

EFFECTS
Overt, untreated maternal hypothyroidism has been associated with an

increased risk of low birth weight and impaired neuropsychologic

development of the off- spring.

However, it is rare for maternal thyroid inhibitory antibodies to cross the

placenta and cause fetal hypothyroidism.

The prevalence of fetal hypothyroidism in the offspring of women with

Hashimoto thyroiditis is estimated to be only 1 in 180,000 neonates.

SUBCLINICAL
HYPOTHYROIDISM
Elevated serum TSH level in the presence of a normal free T4 level
2-5 %
unlikely to progress to overt hypothyroidism during pregnancy in otherwise

healthy women.

Currently, there is no evidence that identification and treatment of

subclinical hypothyroidism during pregnancy improves these outcomes

(30).

Study demonstrated that screening and treatment of women with

subclinical hypothyroidism during pregnancy did not improve the cognitive

function of their children.

INVESTIGATIONS
RECOMMENDATIONS
TSH and T4
Levels of TSH
First Trimester: 0.12.5 mIU/L
Second Trimester: 0.2-3.0 mIU/L
Third Trimester: 0.3-3.0 mIU/L

T3 toxicosis (suspect in overt hyperthyroidism with low TSH and normal

FT4)

No evidence of support routine test of antithyroid antibiodies as it rarely

lead to changes in mx of women who are euthyroid / with thyroid disease.

(antiTPO/antiTG ab). (recommended for Graves Disease in second
trimester)

TREATMENT :
HYPERTHYROIDISM

Thionamide : Propylthiouracil (PTU) or Methimazole

Goal: lowest possible thionamides to maintain FT4 above or in high normal range,
(regardless TSH) Measure FT4 2-4 weekly.

PTU: 50-150mg TDS

Prefered
Inhibits conversion of T4 to T3 and crosses the placenta less readily than methimazole
Hepatotoxicity (routine measurement not warranted)

Methimazole: 10-40mg BD/tds

a/w rare embryopathy : esophageal or choanal atresia as well as aplasia cutis, a congenital skin defect
Less risk of hepatotoxicity

ACOG recommendation: PTU during first trimester, switch to Methimazole beginning of

second trimester

Transient leukopenia in 10% (does not require cessation)

Agranulocytosis (not related to dosage, acute onset)
Discontinue if fever or sorethroat

TREATMENT:
HYPOTHYROIDISM
FT4 replacement: Levothyroxine 1-2mcg/kg daily or 100mcg OD
Post thyroidectomy/radioiodine therapy may require higher dosage

Measured by TSH levels: 4 to 6 weeks interval

Adjust Levothyroxine by 25 to 50 mcg increment until TSH normal

Pregnancy: increase demands of T4 requirement, likely d/t oestrogen

production)

Anticipatory 25% increases in T4 replacement is required.

Preconception counselling

THYROID FUNCTION AND

HYPEREMESIS GRAVIDARUM
Gestational transient hyperthyroidism
Women with hyperemesis gravidarum may have high T4 and low TSH
Thyroid function abnormalities result from TSH receptor stimulation from high

concentrations of hCG.
rarely symptomatic, treatment with thionamide is not recommended
May be a/w multiple gestation or molar pregnancy
Advised for expectant management
Routine measurements of thyroid function are not recommended in

patients with hyperemesis gravidarum unless other signs of overt

hyperthyroidism are evident.

THYROID STORM AND

THYROTOXIC HEART
FAILURE IN PREGNANCY
Acute and life-threatening condition

Hyperembolic state caused by excess thyroid hormone: fever, tachycardia,

cardiac dysrhythmia, and central nervous system dysfunction.

Thyroid storm affects bodys thermoregulatory, cardiovascular, nervous, and

gastrointestinal systems, which leads to multiorgan decompensation

Heart failure and pulmonary hypertension from cardiomyopathy

Decompensation ppt by preeclampsia, anemia, or sepsis
If suspected, therapy should not be withheld pending the results.
Treatment should be carried out in intensive care area within a labor and delivery

unit

Underlying cause should be treated

Avoid delivery in presence of thyroid storm even if fetal status is not reassuring

THYROID NODULE/THYROID
CANCER IN PREGNANCY
Complete Hx and Physical examination, serum TSH, USG Neck
USG neck reliably detects nodules 0.5cm
USG features: Hypoechoic pattern, irregular margins, microcalcifications
FNAC, histologic tumor markers, imunostaining

Radioiodine scanning is NOT RECOMMENDED (risk of fetal irradiation)

However, if there is administration of radioiodine before 12 weeks, fetal

thyroid gland does not become significantly functionally active until 12

weeks of gestation and it does not appear to be at risk of damage.

Thyroidectomy (for malignancies) maybe performed before third trimester

Surgery maybe deferred to immediate postpartum period in women

without aggressive cancer dx in 3rd trimester

POSTPARTUM THYROIDITIS
Defined as thyroid dysfunction within 12 mths of delivery
Evidence of hyperthyroidism (fatigue, irritability, weight loss, palpitations, or heat

intolerance), hypothyroidism (symptoms of fatigue, constipation, or depression) or both

Transient autoimmnue thyroiditis : 5 10% of women during first year after childbirth.
New onset of abnormal levels of TSH and FT4 with 2 phases
1ST PHASE: Destruction-induced thyrotoxicosis
sx caused by excessive thyroid hormone from glandular disruption
Abrupt, small painless goiter
Thyrotoxic phase last a few months.
Treatment of thionamides: ineffective, but may consider beta blockers

2nd phase: overt hypothyroidism 4-8mth post partum

Thyromegaly, hypothyrodism
T4 replacement with Levothyroxine 25-75mcg/d for 6-12 mths

Most resolves spontaneously; 1/3 will develop permanent overt hypothyroidism.

REFERENCE
Thyroid Disease in Pregnancy. Practice Bulletin Number 148, Vol 125, No. 4,

April 2015. The American College of Obstetricians and Gynaecology.

LEO A. CARNEY, JEFF D. QUINLAN , JANET M. WEST, MD, Thyroid Disease in

Pregnancy. Am Fam Physician.2014Feb15;89(4):273-278.

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